220 terms

Step Up to Medicine: Chapter 07 Diseases of the Renal and GU system

young man, firm mass in testicle, painless, preseumed to have testicular cancer until proven otherwise: true or false
Postrenal failure: ARF characteristics
least common cause of ARF
-obstruction of UTI with intat kidney causes increased tubular pressure
-urine produced doesnt get excreted leading to decreased GFR
-blood supply and renal parenchyma intact
-function restored if obstruction relieved b4 damage to kidney
What should a patient do if stone is passed at home?
recover the stone passed - good for analysis and helpful in both treatment and prevention of recurrence
treatment of UtO? what factors (duration, location, cause, duration of obstruction).
if lower: urethral cath for acute onset of obstruction or dilitation with internal urethrotomy if cause is a stricture

if upper: nephrostomy tube drainage = acute...ureteral stent (cytoscope) if there is a ureteral obstruction
When is a renal biopsy indicated?
Only if suspician of acute GN or allergic interstitial nephritis
FSGS as a primary GN
25% causes nephrotic syndrome
-edema, hypoalbuminemia, hyperlipidemia, proteinuria
-HTN, hematuria comon
-variable prog
*do not admin steroids; renal insufficiency 5-10 yrs; progressive

rx; cytotoxic agents; immunosuppressants
CLinical features of ADPKD:
1. ARF
2. Berry aneurysm with intracranial hemorrhaging
3. Down syndrome association - marfanoid hapbitus
-HTN > 50% causes
-PALBABLE KIDNEY on abdominal exam
-CVA complication on PE
penile cancer
incidence peaks in mAles in 70 years
-circumcision is protective and is rare in pts who are
-hsv-2 and hpv 18 infection is risk enhancing
-exophytic mass on penis

tretment is local excision
2 major methods of dialyzing patients
1. Hemodialysis - hospitals/dialysis centers
2. Peritoneal dialysis - CAPD (chronic ambulatory)
Stones that pass spontenous, stones that do not pass spontaneously

Reccurence rate nephrolithiasis
If > 1cm --> will not pass
IF < 0.5 cm then will usually pass

UP TO 50% with recurrences in 10 years of having first stone
Classification of urinary obstruction
1. Acute v. chronic
-sudden onset v. progressive RF/uremia and recurrent inf/bladder calculi
2. Lower v. upper obstruction
-below the ureterovesicular junction = affects urination
-above the ureterovesicular juntion = renal colic and affects concentration
3. Complete verrsus partial obbstruction
4. unilateral v. bilarterall obstrruction
Hereditary nephritis (______) SYNDROME
-xlinked/AD/variable penetrance
-hematuria, pyuria, proteinuria
-hearing los without deafness
-renal failure

No treatment
CRF diagnosis
UA = examine sediment
measure cr clearance to estimated GRF
CBC (anemia/thrombocytopenia)
electrolytes serum
renal US = evaluates the size to r/o cysts
-small kidneys = CR insufficiency w/ little chance to survive
-preseve of normal kidney without excessive CRF
-renal biopsy
How might RENAL ARTERY STENOSIS be diagnosed?
#1 GOLD STANDARD - renal arteriogram (do not use in patients with renal failure 2/2 contrast toxicity

#2 MRA = magentic dye that doesnt cause nephrotoxicity so CAN be used in pts with CRF

#3 Captopril renal scintigram (SCAN); good but non-invasive in pts with good renal function
germ cell nongerminoma testicular tumors:

-embryonic carincoma



-yolk sac tumor
emb- high mlig potential, hemorrhage, necrosis common, mets to lungs and abdominal lymph

chorio is the most aggressive ig mets that have occured by the time of diagnosis

teratoma rarely mets

yolk sac tumor is rare in men but common to boys
Causes of ATN
1. Ischemic ARF
-2/2 severe dec in RBF as in shock, hemorrhagic, sepsis, DIC HF
-ischemia results in death of tubular cells

2. Nephrotoxic ARF
-injury 2/2 to substances that direcly injure renal parenchyma and result in cell death
-antibiotics; radiocontrast agents, NSAIDS
What CRF-endocrine related disorder results in necrotic vascular skin lesions called "CALCIPHYLAXIS"
Hyperphosphatemia secondary to CRF = precipitation of PO43- and Ca2+ leads to vascular compostitions
What are specific measurements for patients with nephrolithiasis?
1. Mild - moderate pain
-high fluid intake, oral analgesics while waiting for stone to pass spontaneously
2. Severe pain with vomiting
-IV fluids, pain control
-KUB and IVP to find set of obstruction
-if not passed in 3 days - urology consult
3. Ongoing obstruction
-surgery necessary
-extracorporeal shockwave lithotripsy
-percutaneous nepholithotomy
signs of early prostate cancer
signs of later prostate cancer
late signs of prostate cancer
asymptomatic ; peripheral and goes central; obstructive symp occurs later bc cancer starts outer and goes inner

symptoms due to obstruction occurs; metastasized to bone and lymph nodes possible with difficulty voiding and increased urinary frequency

bone pain from mets with weight loss, affects the vertebral bodies pelvis and long bones however increases osteoblastic activity
1. GN caused by immunemediated mechanisms
2. Metabolic hemodynamic disturbances
MVP heart abnormality seen in which congenital renal dz?
Pruritis is commonly seen in patients with CRF - what is the treatment?

What is the only CURE to CRF?
Pruritis - capsacician cream, cholestyramine, UV liegh

causes of hyperoxaluria
severe steaorrhea of any cause can lead to calcium oxlate strones due to increased absorption of oxalate

small bowel disease/crohns disease
pyridoxine deficiency
What is orthostatic proteinuria?
patient is standing; has proteinuria, when recombinant, none.

Self limiting/benign
HIV nephropathies 2/2 GN
1. Proteinemia, edema, hematuria
2. Histopatho - looks like FSGS
3, Improves with prednison, ACEi, retroviral
UA findings of renal failure:
1. Prerenal
2. Renal
3. Postrenal
1. Prerenal
Cause: renal artery stenosis
Urine sediment: benign, hyaline
Protein: negative
Blood: negative

2. Intrarenal
Cause: (1-ATN)(2-AGN)(3-AIN)
Urine sediment: (1-muddy brown renal casts, granular)(2-dymorphic RBC with cases, WBC and casts, fatty casts)(3-RBC,WBC,EOSINO, WBC+CASTS)
Protein: (1-trace)(2-4+ protein)(3- 1+)
Blood: (1-negative)(2-3+)(3-2+)

3. Postrenal
Cause: BPH
Urine sediment: Benign +/- RBC
Protein: negative
Blood: negative
Medullary sponge kidney v. Simple renal cyst kidney
MSK: cystic dilitation of collecting ducts
-hematuria, UTI, nephrolithisis
-associated with hyper-pth and parathyroid adenoma
-dx by intravenous pyogram
no Rc necessary - prevent stone formation and treat UTI

Simple cyst
-very common (50% > 50YO); incidence increases with age;
-may be single, may be multiple
-asymptomatic, discovered incidentally
DO NOT treat
Why might there be a delay recovery of epithelial cell function relative to GFR in pts with ATN?
2/2 tubular cell damage with prolonged osmotic diuresis due to retained solutes during the oligo phase
Imaging of nephrolithiasis
1. Plain radiograph of kidney, ureter, bladder (KUB)
-initial imaging detecting stones that are ca-ox/caphos/struvite/uric acid but NOT able to note cysteine stones

2. CT scan without contrast (spiral) - most sensitive and detects all stones

3. IVP - degree/extent of UTO - decides whether or not pt should have surgery

4. Renal ultrasonography - hydronephrosis/ureter obstruction
Limitations/complications with dialysis
1. Doesnt replicate kidney synthetic function of EPO and VITAMIN D

1. Hemodialysis
-hypotension often causing MI and fatigue
-hypo-osmo of ECF compared with BRAIN = n/v/headache
2. First use syndrome
3. Anticoagulation
4. Infection
Pathophysiology of CRF:
1. Plasma cr vaires inversely with GRF
2. Cr clearance is most common clinical measure of GFR
3. Inc plasma cr indicates disease progression; dec plasma Cr indicates recovery of renal function
4. > Africa americans than caucasians
What is azotemia?
Progosis of ARF:
Elevated BUN and Cr
-increase BUN = catabolic drugs (steroids); GI/soft tissue bleeding, dietary protein
-increase creatinine = increased muscle breakdown and various drugs (baseline or level varies proportionally with muscle mass)
Membranous GN
Nephrotic syndrom: proteinuria, hypoalbuminemia, hyperlipidemia
-thickened glomerularocapillary walls; primary dz idiopathic, secondary disease d/t infection (HCV/HBV/syphilis, malaria)
-drugs - gold, captopril, penicilamide)
-neoplasms or lupus can result in DN

Rx: remission (40%)/RF(33%) steroid therapy
How might fanconis syndrome be treated for?
-ALkali/salt supplement

WHY? bc the proximal tubulae cannot administer glucose or resorb it (AA, Sodium, potassium, phosphorus, UA, HCO3-)
Struvite strones
radiodense and visible on KUB
rectangular prisms

Recurrent UTIs = urease + organisms (proteus, enterobacter, serratia, klebsiella)

Facilitates by an ALKALINE URINE (which is seen in patients with RTA 1 and 2) and urea splitting bacteria that convert urea into ammonia

Ammonia thus combines with excess mg2+ and phos 2+ and forms struvite staghorn stone
WBC Casts are indicative of a ______ ________ inflammation due to a type of ________
renal parenchymal (inflammation) due to a type of INFECTION
Proteinuria is decribed as the urinary excretion of >____mg/protein/24hr.
4 major classifications:
>150 mg protein24hours

1. Glomerular
2. Tubular
3. Overflow proteinuria
4. UTI, Fever, CHF, prenancy, orthostatic proteinuria
How are uric acid stones diagnosed if not picked up on XRAY?
elevated release of pruines
-see on CT, US, IVP for detection
-will treat with allopurinol for prohylaxis TLS and will treat with rasciabine to break apart the already formed urate if leukemic pt undergoing chemo
causes of lower tract obstruction
Bph, prostate cancer
urethral stricture, stone
neurogenic bladder (ms) or DM
bladder ca
secondary glomerular disorders
Diabetic nephropathy
HTN nephropathy
Good pastures
sc nephropathy
HIV nephropathy
GN in endocarditis
Fluid and electrolyte disorders in patients with CRF
-volume overload
-hyperkalemia - decreased urinary secretioin
-hypermagensiemia - 2/2 urinary dec secretion
-metabolic acidosis (loss of renal mass, dec ammonia production and kidneys cannot exeed H+)
What treatment (anti-htn meds) are contraindicated in patients with RENAL ARTERY STENOSIS?
ACEi because will dilate the efferent arteriole and further decrease GFR and increase RBF - the GFR is already below normal 2/2 RAS so wouldnt want to exacerbate
Clinical features of CRF:
1. CV
2. GI
3. Neurologic
4. Hematologic
5. Endocrine
6. FLuid/electrolytes
1. CV: HTN, secondary to sodium retntion; dec GFR, increased RAAS, increased BP
2. CHF = volume overload; HTN; anemia; pericarditis = uremic
3. GI = due to uremia (n/v) loss of apetitie
4. NEURO = lethargy, comnlence, confusion, peripheral neuropathy, uremic seizures (asterixis, hyperflexia0; restless leg, Hypocalcemia
5. Heatologic = normocytic, normochromic anemia (dec EPO)
6. Endo = Ca2+/PO4- distubance
7. Volume overload: hyperkalemia; elevated mag; elevated phos; decreased pH
Advantages v. disadvantages of hemodialysis
Advantages: more efficient than peritoneal dialysis; high flow rates and efficient dialyzers short period of time required for dialyisisl QUICK to initiate than peritoneal use of temp vascular access in emergency

Disadvantages: less similar to function of natural kidney; increased hypotension to rapid change in volume; hypo oSmo 2/2 rapid removal of solute; regular vascular access
Intrinsic renal failure (ARF)
Kidney tissue is damaged such that glomerular filtration and tubular function are significantly impaired and tubular function are significantly impaited and cannot concentrate urine efficiently

Causes: ATN, GN (good pastures, wegeners, post GN), Vascular Dz(renal artery occlusion -TTP/HUS), Intersitial Dz (allergic intersisital nephritis)
Sickle cell nephropathy
sickling of RBC in microvasculature leads to renal infarction in the papilla
-recurrent papillary infarct leads to papillary necrosis and renal failure and UTI
Prostate cancer:

95% adenocarcinomas

rf include that of:
AA race
high fat diet
positive family history
exposure to herbicides or pesticides in certain occupations including farming and chemical industries
Clnical features of glomerulonephropathies
impairment of selective filtration of blood - increased excretion plasma proteins and blood cells

as disease >>, GFR dec --> renal failure

Proteinuria and hematuria
Which disease commonly associates with
-intracranial berry aneurysm
-abormal heart dz (MVP)
-cysts in other locations in body (liver, pancraease, brain)
-renal failure ain 50-60YO patienst
What is overflow proteinuria?
increased production of small proteins that overwhemlms tubules ability to reabsorbs them. BJ protein in MM good ex.
if a patirnt has an acute obstuction, next step?
emergent dx test: renal US, excretory urogram
immediate intervention
Post-streptococcal GN = #1 cause of ____ ______
NEPHRITIC syndrome
1. occurs 10-14 post streptococcal infection by GAS

Population: children 2-6YO
-hematuria, edema, HTN, proteinuria; dec complement; elevated ATO
-self limited (wks to MO) - good Px
can become RPGN in adults

Treatment: antiHTN, loops for edema; noAB
What is the most common cause of secondary HTN?
Renal artery stenosis
-decreases blood flow to the JGA thus the RAAS becomes activated and vasocontricts the effecrent arteriole and releases aldosterone for H2o resorption, etc.
Whenever a patient presents with elevated Cr levels, what is the first thing to do when diagnosing or patients with CRF or ARF?
Determine the baseline creatinine (cr)
-determines if ARF, CRF, Chronic RF/imposed ARF ("acute on chronic"
Frequency and access in CAPD versus that of HDialysis?
Diasylate fluid drained/replaced each HR in acute peritoneal, but 1x 4-8 hours in CAPD

Access CAPD: diasylate infused into peritoneal fluid by catheter. If acute PD, temp catheder used
Atheroembolic disease of the RENAL arteries
Cholesterol crystals dislodge from plaques in large arteries and embolize in the renal vasculature (cholesterol emboli syndrome is similar)

-can occur in retina, brain, skin
when might a cystourethirography be indicated for use?


CT scan?
lower tract obstruction

evaluate urethra and or bladder

cause of obstruction
Prognosis of ARF?
>80% of patients in whom ARF develops never completely.

Older patients have decreased recovery = #1 cause of death - infection
Minimal change disease
1. Nephrotic = edema, proteinuria, hyopalbuminemia, hyperlipid
2. most common to children
3. most common to NHL and Hodgkin association
4. No histological changes on light microscopy - fusion of foot processes on EM
4. Excellent prog with treatment of steroids 4-8 weeks relapses common
When is a renal US useful?
1. Kidney size ,function --> r/o UT obstruction (ex: postrenal failure)
-bilateral hydronephrosis
-hydroureter; BPH

2. Order for pts with ARF unless obvious that patient doesnt have postrenal failure
ADPKD = Renal cystic disease
Autoimmune DOM condition
-variable course, EDRS commonly develops in 50% of patients by age 50-60s but remainder have normal lifespan
risk factors for testicular cancer?

- surgical correction doesnt eliminate risk

klinefelters sydrome
- xyy

painless mass or lump; firmness of testicle beacuse of lack of pain that goes unnoticed until advanced
Hyaline casts are seen in ____ ______
Pre-renal failure
How might amyloidosis occur in patients on dialysis?
Hemodialysis - associated amyloidosis of B2 macroglobulin in BONES and JOINTs
What is the renal failure index if >1% or if <1%?
Urine sodium
-Ucreatinine/Pcreatinine x 100 = RF index
-Values <1% = prerenal failure
-Values >1% = ATN (intrinsic)
What are uric acid stones?
account for 10% of all renal stones and cause:
1. hyperuricemi, secondary gout/chemotherapy via TLS for lymphoma and leukemias
-release of pruine from dying cells is what causes the elevated uric acid
-flat [ ] plates; stones (not seen onXRAY)
What is renal failure
rapid decline in renal function with an increase serum creatinine level (inc 50% or absolute 0.5-1.0 mg/dL)

urine output can be (oligouric, anuric, nonoligouric) - severe arf occurs without a decrease in urine output
Characteristics of UT obstructions
Leads to renal insufficiency and hydronephrosis (dilation of UT = pelvis and calysis)
More common in males 2/2 BPH and prostat CA
UTO doesnt cause ARF unless obstruction is bilateral OR prior damage occurs
Nephrotic v. Nephritic

-patho: abnormal GN permeability
-causes: many conditions; MGN = #1; then DM, HTN, SLE, RX, FSGS/MCD
-labs: Proteinuria <3.5 g hypoalbumin/hyperlipid
clinical: edema, hypercoag, hyperlipidemia, hypoalbuminemia, inc infection risk

-patho: inflammation of glomeruli due to any cause of GN
-post streptococcal GN #1
-hematuria, HTN, ARF (azotemia, oligouria); proteinuria
how might renal cc be diagmosed versus rx.
renal us to detect the mass v cyst
abdominal ct to determine shape and stage

- radical nephrectomy excision of kidney and adrenals influding gerotas fascia with excison of nodsl tissue at renal hilum for stage
Prognostic factors to consider in ARF
1. Severity - magnitude of inc cr; oligouria;excretion of sodium; req of dialysis; duration of renal failure; abnormalities on UA
2. Health of patient - age, presense, severity, reversibility of disease
3. Clinical circumstances - cause of RF; # failed organs
What are the CLINICAL FEATURES of someone with renal artery stenosis (will result in AKI prerenal)
1. HTN - will be sudden in onset with a pt lacking a significant family hx. Severe HTN (may become malignant and refractory medical therapy)

2. DECREASED renal function. Will have a BUN:Cr <20:1 will have a FENa of <1% and will have low urine sodium

3. ABDOMINAL BRUIT = RUQ if right kidney; LUQ if left kidney or epigastrium
Which calcium/phosphorus disturbances occur in pts with CRF?
Pts with CRF are unable to readily clear phosphorus therefore becomes hyperphosphatemia; which results in dec renal production of 1,25D3. Thus HYPOcalcemia causing 2ndary hyperpTH, increased PTH

Hypocalcemia, hyPERphosphatemia, but longstanding secondary hyperPTH and calcium based phosphate binders cause = HYPERCALCEMIA

secondary type PTH = renal osteodystrophy (bonepain/bonefractures)

Hyperphosphatemia = Ca2+, increase phos to precipitate, increased vascular calcification causing skin resins.
How is the patients blood retrieved (on hemodialysis)
1- central catheder placed in th subclavian vein for temp access
2 - AV fistula - #1 form of permanent dialysis artery and vein to forearm; requires CV surgery to connect the RADIAL ARTERY and VEIN to one antoher in forearm - 6 weeks to mature and heal - audible bruit over the fistula = PATENT, so this is a good thing.
3 - implantable graft
Nephrosclerosis due to HTn is the SECOND most common cause of ESRD, what is the first most COMMON cause of ESRD?
HTN 2/2 DM = most common
HTN 2/2 nephrosclerosis = 2nd msot common
RPGN is a clinical syndrome that includes any type of GN in which a rapid (acute) deterioration occurs over _____ to _____ Outcome:
ESRD and RF = outcome
transitional cell carcinoma accts for ____% od bkadder cancers

squamous cell carcinoma accts for ____%

adenocarcinoma accts for _____%
What clinical assocations are seen with folks with ADpkD
#1 intracerebral berry aneurysm in 5-20% of cases
#2 Diverticula (colon
#3 Infection of hte renal cysts; bleeding into cysts
#4cysts on other organs (liver, spleen, pancreas, brain)
#5renal failure (late)
#6 kidney stones
#7 heart abnormality
Glomerular diseases
two broad categories:
1. Intrinsic patholgy (primary)
2. 2/2 DIT systemic disease

-present with nephrotic syndrome or nephritic syndrome
-duration varies (days to weeks) - acute GM disease and years if CHRONIC
Treatments of ARF generally:
1. Avoid rx: decreases RBF like NSAIDS; nephrotixic: aminoglycosides, radiocontrast agents
2. adjust doses of medicibes depending upon renal fcn
3. Correct fluid balance - if dehydrated = IV fluids; if overload = loops or dialysis monitor by day weight
4. Correct electrolyte imbalance
5. Optimize cardiac output BP 120 to 14/80 to 90
6. order dialysis if uremia, hyperK
Asymptomatic proteinuria
1. Transient
2. Persistent
Transient: excellent prognosis (without further eval)

Permanent: req workup to r/o renal disease
Most common sites of nephrolithiasis
development of stones within the urinary tract
1. Ureterovesicular junction = #1
2. Calyx of kidney
3. Ureteropelvis junction
4. Intersection of ureter and liac vessels
How might a urine chemistry distinguish between different forms of ARF?
1. Urine Na+ depends upon sodium intake
2. FENa: collect urine and plasma electrolytes simultaneously (Usodium/Psodium)/(Ucrt/Pcrt) x 100

If <1% then prerenal
If 2-3% = intrinsic or ATN - FENa useful if oligouria present
What are two major associateition with hyperparathyroid and parathyroid adenoma/
Medullary spondge kidney
Urinalysis of nephrotic syndrome can reveal?
1. Proteinuria with dipstick
2. RBC casts if GN; WBC casts if peylonephrotis and interstitial nephritis; fatty casts sugest nephrotic syndrome due to lipiduria
3. If UA confirms protein, perform 24 hr urine collection (alb and Cr) to establish presense of proteinuria
prostatic cancer treatment
if localized to prostate then
- radical prostatectomy or watchful waiting in older males who are asymptomatic

if locally invasive then
- radiatino therapy plus androgen deprivation
- no cure just decreases spread

if met
- then decrease testosterone
- perform orciectomy and anti-androgen therapy
- LRH agonist ----- LEUPROLIDE
What is the GFR of:

2. Moderate CRF
3. Severe CRF
1. 70-120 mL/min
2. 30-70 mL/min
3. <30mL/min
4. <10mL/min
Advantages CAPD v. Disadvantages CAPD
-dialysis done independently
-mimics physiology of normal kidney

-high glucose can cause hyperglycemia and hyper TG
-increased abdominal girth
When might a renal vein thrombosis be seen?
1. Nephrotic syndrome
2. Invasian of the RV by that of RCC
3. Trauma
4. Pregnancy/oral contraceptive
5. extrinsic compressions (retroperioneal fibrosis, AORTIC abominal aneurism, LAD, dyhydration
diagnosis v treatment of bladder cancer
-ua/uc to rule ut infection
-urine cytology that detects malignant cells
-cystoscopy biopsy - definitive
-cxr/ct scan to stage

0-superficial limited to mucosa in situ
a-transurethrll resection of bladder tumor
b-muscle invasion
c-extends periumb fat
d- mets
Fanconi's syndrome
Hereditary/aquired proximal tubule dysfcuntion leading to defective transport of GLUCOSE/AA/sodium?K/PHOS/UA/HCO3-.

Leads ultimately to glucosuria, phosphaturia (RICKETS) with imapried ffrowth, osteomalacia (osteoprorosis), proteinuria, polyuria. RTA (HCO3-); elevated Ca2+ urinae, decreased K+ serum
Treatment of
1. Asymptomatic transient proteinuria
2. Asymptomatic persistant proteinuria

3. Symptomatic proteinuria
1. Asymp + transient = no further workup
2. Asymp + transient = check BP; UA; LDL/HDL

3. Testings:
-treatment disease = DM, MM, SLE, MCD
-ACEi = decrease albumin loss and prog]]ress of nephrotiosis. Essential if CRF with DM and HTn and should be admin b4 fixed albuinuria present

4. Diuretics, dec protein
5. Vaccine - pneumococcal, influenze
Hartnup syndrome
AR inheritance of defective amino acid transporter
=doesnt reabsorp that of tryptophan and other neutral AA - resulting in nicotinamide deficiency = pellagra, glossitis, diarrhea, dermatitis, ataxia, death
=administer supplemental nicatinamide to symptomatic patients
RBC cases are indicative of a _______ disease
glomerular (nephritis)
Complications associated with peritoneal dialysis?
peritonitis = cloudy fluid fever, abdomenal pain
abdominal/inguinal herniation
hyperglycemia = DM pts especially
protein malnutrition
Forms of reversible ARF on restoration of blood flow - but if reperfusion dont occur or hypoperfusion persists - then ischemia results and leads to _____.

Pre-renal failure v. ATN?
Acute tubular necrosis (ATN)

Pre-renal failure:
1. Urine osmo: >500
2. Urine Na+: <20
3. FENa: <1%
4. Urine sediment: scant

1. Urine osmo >350
2. Urine Na+ > 40
3. FENa >1%
4. Urine sediment: full browish pigment graular casts with epitherlial casts
What are struvite stones and what are they made up of?
Mg-Phos-Ammonia stones in which can become "staghorn"
-seen on XRAY
-rare but can occur
Risk factors fo RCC
cigarette smoking like that for pancreatic CA
phenacetin analgesics in high doses
chronic dialysis ife multicytic kidney disease
heavy metals including mercury and cadmium
Differentiation between CRF and ARF
Chronic - hx of kidney dz, HTN, abonormal UA, edema
-small kidney on US
-irreversible damage
-hyperK, acidemia, phosphatemia, anemia
-UA broadcasts >2-3 WBC

-normal function returns
-hyperkalemia, acid, hyperphos, anemia
Why might HYPERLIPIDEMIA be seen in patients with increased hepatic synthesis of albumin 2/2 nephrotic syndrome (hypoalbuminemia)
increased hepatic LDL/VLDL because increased albumin
RTA type I
-inability to secrete H+ at distal tuble; thus new HCO3- cannot be produced
-inability to acidify the urine = metabolic acidosis
-urine pH >6 (normal is 4.7) therefore if urine pH is > 4.7 then assume urine "alkalosis"
-inc ion excretion of (sodium, ca, K, sulfate, phosphate)
-dec ECF, hyPOkalemia; renal stones/neprhocalcinosis 2/2 elevated calcium phosphorus imbalance
Azotemia v. Uremia
azotemia: increased BUN

uremia: signs and symptoms assciated with accumulation of nitrogenous wasts due to impaired renal function. Occurs when BUN > 60mg/dL
Alternative to traditional hemodialysis
continuous AV hemodialysis (CAVHD)
continuous venovenous hemodialysis (CVVHD)

used in hemodynamically unstable patients like ICU patients with ARF
-low flow rate of blood and diasylate enable dialysing dialysis to occur while dec rapid shift in volume and osmolarity.
-require highly efficient dialyzers to be effective
Pathophysiology of ARF
Dec clearance of metabolits (BUN, Cr, Uremic toxins)

renal parenchyma is undamaged, tubular function (there the concentrating ability) is preserved. Thus, the kidney responds appropriately - conserves as much sodium and water
In rare cases, ++++++++ can cause malignant HTN
bladder cancer chracteristics
bladder carcinoma is the most common type of tumor in the GU with 90% being transitional cc

occurs from kidney to bladder but 90% in bladder

route of spread is local to tissues

recurs post removal
Causes of atraumatic cases of hematuria?
25% infections (cystitis, urethritis, prostatitis)
20% kidney stones, bladder malig/RCC; glomerular DZ IgA nephropathy; trauma = foley cath, blunt trauma; strenuous exercise (marathon) fever; systemic disease (SLE, RF, HSP, WG, HUS, GPS)

bleeding d/o, rx, ADPKD, BPH
Type I RTA v. Type II RTA
Type 1: distal
-hypok, hyperchloremic
-metabolic acidosis
-nephrolithiasis (ca2+ and phos binding)
-Rx: HCO3-

Type 2: proximal
-hypok, hyperclor
-ma w/out ag
-no nephrocalcinosis/lithiasis
-dont treat w/ bicarb bc is not being absorbed proximally
-urine alkalosis
-Rx: Sodium restrictiong will inc Na+ resorption and HCO3- in urine
Fatty cases in urine indicative of a ______ syndrome
Glomerular proteinuria v. Tubular Proteinuria
-increased glomerular permeability to proteins - becoming nephrotic
-seen in GN
-more severe protein loss

-small proteins filtered at glomerulus then reabdorbed by tubules appear in urine d/t abnormal tubules (ATN)
-less severe = DIT: sickle cell, UT obstruction, interstitial nephro
What are the complications in early phase of ARF?
1. ECF volume expansion --> pulmonary edema
-treatment with that of FUROSEMIDE

2. Metabolic = hyperkalemic: dec K+ excret and movement of K+ from ICF-->ECF due to tissue destruction & acidosis. 2. Acidosis = inc anion gap d/t H+; if <16 - use sodium bicarb. 3. Hypocalcemia - dec vitamin. 4. Hyponatremia 5. Hyperphosphatemia. 6. Hyperuricemia
Risk factors involved with nephrolithiasis?
1low fluid intake = #1 risk factor
2. family history
3. GOUT/CROHNS/hyperPTH/TypeIRTA(distal)
4. Medications: loops, acetazolamide, antacids, chemotheraputic treatment that cause cell to be brown (uric acd stones)
5. Males (3x more likely)
6. UTI (especially with urease-producing bactrim)
PSA asy is refined due to
1. age adjusted psa because will increase with age
2. PSA velocity is the analysis of the rate of increase in levels overtime
3. free v. bound serum PSA
-psa produced by prostate cancer is plasma protein bound
-psa produced by normal cells = free PSA
4. PSA density = correlation of psa levels with prostate volume
Causes of nephrotic syndrome
1. Primary glomerulonephritis disease (50-70%)
a. Membranous GN most common
b. FSGS (25%) - HIV
c. Membranoproliferative CN (15%)
d. Minimal change disease (75%) children
2. Systemic diseases: DM; CVD; SLE; RA arthritis; HSP; PAN; Wegeners
3. Amyloidosis.cryoglobulinemia
4. Medications: Captopril (ACEi), heroin, metal, NSAIDS, penicillamide
5. Infection = b, v, protozoal
6. Malignant, HTN
Chronic interstitial nephritis
slowly progressive IN leading to fibrosis ESRD over the years
-renal papillary necrosis can be present
-no signs of hypersensitivity like AIN
-causes = prolonged UTO reflux nephropathy, heavy analgesics use, ?lead/camin"; arterioar nephroschlerosis with HTN.
chronic renal failure differs from RF in which ways?

2 most common causes?
1. Irreversible
2. Progressive loss of GFR happening months - years

1. DM (30%)
2. HTN (25%)
3. Chronic GN (15%)
4. Interstitial nephritis
6. Obstructive
7. Delay in ARF rx
Process of peritoneal dialysis
1. Peritoneam = dialysis membrane
2. Infuse diasylate into peritoneal cavity and fluids/solute from peritoneal capillaries diffuse into fluid diasylate and is then drained from abdomen
3. Hyperosmolar (HIGH GLUCOSE) solution used and water is removed from blood by osmosis
Pre-renal failure
#1 cause of ARF = potentially reversible
etiology-dec systemic arterial blood volume or renal perfusion
-hypovolemia = dehydration, excessive diuretic use, por fluid intake, vomiting, diarrhea, burns, hemorrhage
-peripheral vasodilation = sepsis, excessive antiHTN meds
-renal arterial obstruction
-hepatorenal syndrome
Renal vein thrombosis clinically presents with
decreased renal perfusoin -->ESRD
flank pain

1. renal venography visualizing occluding thombosis
2. IVP
3. Anticoagulation therapy to prevent PE
Postrenal rx in ARF
bladder catheder inserted to decompress the urinar tract. Get urology consult
testicular cancer

men 20-35 yo
high cure rate


1. germ cell tumor - 95% all testicular ca - 20-40 yo; cure > 95%
-seminoma -35% slow growth and radiosensitive
-nonseminoma -65% mixed cell ; choriocarcinoma; teratoma; yolk sac
2. nongerm cell tumor 5%
-leydig cell tumor
-sertoli cell tumor
Tests used to determine etioogy of nephrotic syndrome?
Creatinine clearance = best test of renal function
Serum BUN/Cr
CBC - detects anemia d/t renal fail
Serum albumin level
renal US - obstruction, mass, cystic dz
IVP - chronic pyelonephritis
ANA- lupus; antigbm; hepatitis serology; antistrepto AB titers, complement levels
serum and urine electrophoresis (myeloma)
Diagnosis of ARF is usually made by finding elevated ____ and ______ but is asymptomatic
Type 4 RTA
1. any condition of hypoaldosteronism or inc renal resistance to aldosterone such that doesnt allow intercalated A or B cell of collecting duct to fcn, therefore no secretion of H+ from urine.

If interstitial renal dz, DIABETIC nephropathy decreases sodim absorption with dec H+/K+ secretion at distal tubule. Therefore will be HYPERKALEMIA (retention of K+) and urine acidosis
3 tests for POSTRENAL failure
1. Physical examination - palpation of the bladder
2. Ultrasound - look for obstruction, hydronephrosis
3. Catheder - look for bleeding
Diagnosis of ARF
1. Blood tests
a. increased BUN/increased CR levels
b. electrolytes (K+, Ca2+, PO4 3-), albumin levels, CBC with diff

2. UA
a. dipstick (+) for protein (3+ and 4+) suggests intrinsic renal failure due to glomerular insult
b. Microscopic examination of urine sediment is very helpful

3. Urine chemistry
4. Urine culture
5. Renal US
6. CT Scan
7. Renal biopsy
What is "first use syndrome"
chest pain
back pain
anaphylais post new dialysis machine
Lab findings of acute renal failure --> PRE-RENAL
1. Oligouria - always found in prerenal ARF (This is to preserve volume)
2. Elevated BUN to serum creat ratio = >20:1 ratio - hence the kidney can reabsorb urea.
3. Elevated urine osmolality *>500mOsm/kg water because the kidney can reabsorb H20
4. Decreased urine sodium (<20mEq/L with fractional excretion of sodium <1%) beacuse sodium is avidly resorbed (FENa <1%)
5. Elevated urine/plasma Cr ratio (>40:1) filtrate is reabsorbed
nonseminoma disease treatment for testicular tumor
orchiectomy and retroperitoneal lymph node dissection
Of the 4 types of renal stones, which is most common?
Calcium stones (80-85%) = calcium oxalate and calcium phosphate
-biconcave ovals
-radiodence (seen on KUB!)
Acute renal failure can be divided into:
I. Pre-renal (40-80%)
-causes: volume loss/sequestration, decreased cardiac output, hypotension
II. Post-renal (10-30%)
-causes intrarenal: crystals/proteins
-causes extrarenal: pelvis/ureter/bladder/urethra
III. Renal (5-15%)
-glomerulonephritis/vascular disorder/interstitial disorder/ATN
What are the clinical features of RCC
gross hematuria is the most common sxs in 70 % of pts

adominal or flank pain in 50% of pts

adominal or flank mass in 40% of pts

wt loss plus fever

paraneoplastic syndromes (epo, pth like with elevatd calcium, renin (2 htn), cortisol (2 cushings)
Nitrates in urine v. leukocytes esterase
nitrites = bacteria in urine
leukocye esterase = WBC in urine
What is renal papillary necrosis?
analgesic nephropathy (pathology to the nephron); DM nephropathy; SCD, UTO, UTI, alcoholism, renal transplant rejection

Dx: excretory urogram will show changes in both the papilla and medulla
treatment: sloughed, necrotic papilla causing urethral obstruction; treat cause and STOP offending agent
Process of hemodialysis:

How frequent?
-blood pumped to articial dialyzer outside of body through dialyzer, typically consisting of fine capillary netweoks of the semipermeable membranes. The diasylate flows on OUTSIDE of networks and fluid/solute flows on/across the membrane and re-enters circulation.

Frequency: most hemodialysis pateints require 3-5 hours of dialysis 3 days per week.
what is orthostatic proteinuria?
occurs most often in <30 yo patients
-3-5% teens affected
- dx by UA microsopy, urine protein, 24 hr collection with inc protein excretion in the upright position but normal when supine (< 50 mg/8 hr)

ex: LRV entrapment or nutcracker syndrome occurs by the entrapment if the left renal vein by the aorta and sma may be the cause

treament is benigh
Hypertensive nephrosclerosis defined:
-systemic HTN with increases capillary hydrostatis pressure in the flomeruli leading to benign/malignant sclerosis

1. Benign nephrosclerosis: thickening of the glomerular afferent arterioles; develops in pts with longstanding HTN
-mild-moderate increase in creatinine levels with microscopic hematuria; protein + in urine
2. Malignany nephrosclerosis: longstnding benign HTN/undiagnosed pt will because malignant.
-dec renal function and accelerated HTN 2/2 diffuse intrarenal vascular injury
-increased in AA
-elevated BP: papilladmia, cardiac decomp; CNS changes
-renal (inc CR, proteinuria, hematuria, RBC/WBC casts, nephrotic syndrome
Dialyzable substances
ethylene glycol
magnesium-containing laxatives
3 types of ARF
1. Prerenal = decrease in RBF (60-70%) of cases
2. Renal = damage to renal parenchyma (25-40%) cases
3. Postrenal = UT obstruction (5-10%) cases
Which meds in patients with decreased perfusion causes precipitate prerenal failure?
risk factors for bladder cancer
cigarette smoking
industrial carinigens anx aniline dye or azo dye
radiation, biologic agents, coffee sweeteners
lt use of cyclophosphamide causes hemorrhagic cystitis
diagnosis of hematuria
1/ urine dipstick
2/ UA - look at sediment (RBC casts - interstitial/tubular/GN); pyuria (send urine culture) (+) blood, but no RBC think hemoglobinuria/myoglobinuria
3/ UA specimen = CYTOLOGY to detect CA
4/ 24 hour urine = treatment for Cr and protein to look at RF
5/ Blood tests
6/ IVP, CTScan, US if above doesnt dz
7/ renal biopsy last dx test
RTA type II
Defect in the ability to reabsorb HCO3- at the proximal tubule, inc in HCO3- excretion of bicarbonate in the urine and metabolic acidosis. Losses of K+ and Na+ in urine

1. Hypokalemia
2. Hyperchloremic non-anion gap metabolic acidosis
2 most common mortal complication of early ARF:
1. Hyperkalemia cardiac arrest
2. Pulmonary edema
diagnosis of testicular cancer
1. PE - palpable testicular mass
2. Ultrasound- intial test for localizing tumor
3. Markers-
-bHCG always elevated in choriocarcinoma and may be elevated in other nonseminomatous germ cell tumors like embry or teratoma or yolk sac
-AFP increasd in embryonal tumors 80% - never seen in chorio or semino

4. ct scan cxr for staging
Outcome of patients with sickle cell nephropathy
Nephrotic syndrome can develop which leads to renal failure
ESRD (50%)
Ischemis injury occurs, increases risk of dehydration (imparing urine concentration)
Sickling crisis

Treatment: ACEi is best
how are the electrolytes abnormalities treated in patients with CRF?
1. hyperphosphatemia - with ca2+ citrate (calcium citrate) = phos binder
2. pteitns with CRD treatent with :T pra; ca;cium and vitamin D to allow decreated seoncary hyper PTH and uremic osteodystrophy
3. acidosis - treatment underlying cause (RF) and administer bicarbonate
Treatment if history of renal stones:
HCTZ - if hypercalcemia or hypocalcuria

Allopurinal - if uric acid stones

either way - DRINK MORE WATER!
stages of prostate cancer
1. nonpalpable and confined to prostate
2. palpable nodule but confined to prostate
3. extends beyond capsule but no mets
4. mets
Diagnosis of nephrotic syndrome
1. UA - dipstick and read colors
a. albumin - detects concentration of > 30 mg/dL or higher
b. graded 0; trace; 1+ (15-30 mg/dL) through 4+ (>500 mg/dL)
c. more sensitive to albumin than Ig; thus can be false (-) if urine protein is globulin (light chains) in MM

2. Urinalysis
3. Microalbuminuria
Clinical features of AIN:
Causes ARF
-rash, fever, eosinophilia
-pyuria, hematuria

Dx: if pt knownto have offending agents and has the following:
RASH, fever, AR insufficiency + eosinophils - think AIN
High post residual volume can result post overflow incontinence 2/2?
autonomic neuropathy of detrouser m of bladder
How can RAS be treated?
1. REVASCULARIZATION with percutaneous renal angioplasta as the inital treatment in the majortiy of patients (PRTA)
- the > success in pts from FM dysplasia than atherosclerotic patients

2. Surgery is PTRA doesnt work (BYPASS)
3. Conservative treatment therapy (ACEi, CCB) alone if PRTA and surgery are contraindicated
Absolute indications for dialysis "AEIOU"
1. Acidosis - significant, intractible, metabolic acidosis
2. Electrolytes - severe persistance hyper K
3. Intoxications - methanol, ethlyne glycol, lithium, ASA
4. Overload - hypervolemia not managed by other means (furosemide)
5. Uremia - clinical presentation, not lab values, uremic pericarditis = absolute
Diagnosis of kidney stones (nephrolithiasis)
1. UA - microscopic/gross hematuria
2. reveals associated UTI if pyria/bacteria is present
3. examine the urinary sediment for crystals - CA2+/ammonia+mg+phos/struvite stones, cystine, UA stones)
4. Determineurinary pH = alkaline urine indicates urease + bacteria (struvite) that can lead to infection OR can indicate possible renal tubular acidosis
5. ACIDIC urine is USUALLY indicative of renal stones
6. Urine culture
7. 24hr urine
8. serum chemistries
painless hematuria and dysuria frequency
bladder cancer
What is an IVP?
Intravenous pyelogram used to diagnose pyelonephritis
Treatment of CRF
1. Diet - low proteiin (0.7-0.8 g/kg) - use low salt diet (HTN, CRF, OLIGO) - restrict K+ and phos/mag
2. ACEi = dilates efferent arteriole so ^RBF and ^GFR and dec rate of ESRD
3. BP control = strict control to dec rate of prog ACEi are preferred agents
4. Glycemic control = prevents worsening if DM
5. Correct electrolytes
6. Anemia - rx EPO
7. Pulmonary edema = dialysis
What makes type IV RTA different from type I and II?
Type IV: hyperkalemia/acidic urine
Type I/II: hypokalemia/alkalosis of urine

BUT both still results in metabolic acidosis with non anion gap
Prerenal treatment
1. underlying disorder
2. give NS to maintain euvolemia and restore BP but not to pts with edema/ascites
3. stopping antiHTN treatment - eliminate offenders ACEi/NSAIDS
4. If UNSTABLE = use swan-ganz monitoring for assessment of intravascular volume
treatment for testicular cancer
1. removed surgically to confirm diagnosis by inguinal approach because a scrotal incision may lead to tumor seeding of the scrotum

2. post orchiectomy, peorm a ct scan of chest abdomen and oelvis for staging
3. bHCG and AFP measurement post orchiectomy and for comparison
4. further trestment is dependent upon histology
Postrenal obstruction, if untreated, can lead to?
Acute tubular necrosis
Treatment of nephrolithiasis
1. Analgesics: morphine IV, parenteral NSAIDS (ketorlac)
2. Vigorous rehydration: beneficial in ALL forms of stones
3. Antibiotics = it + pyuria
4. Outpt management for most pts; hos admission if pain is not controlled; anuria; renal colic + UTI and or fever; strone > 1cm and unlikely to pass spontaneously
RCC characteristics
twice as comon in males than in females
- sporatic with less than two percent 2/2 autosomeal dominant VHL syndrome
- cause is unknown
- area of mets = lungs liver brain bone
Key features of nephrotic syndrome
1. Proteinuria (>3.5g/24hrs --> 2+)
2. Hypoalbuminemia (hepatic albumen syn cannot kep up with the protein loss renally) - leads to decreased plasma oncotic pressure leading to edema
3. Edema (pedal edema, periorbital, anasarca, ascites, effusion). dec albumin, increased aldosterone
4. Hyperlipidemia
Renal tubular acidosis
RTA disorder of renal tubules leading to nonanion gap hypercloremic metabolic acidosis:

-decreased H+ excreted in urine leading to acidemia and urine alkalosis with MeTABOLIC acidosis

Types: 1, 2, 4
testicular torsion v. epididymis
testicular torsion is a surgical emergency (<6hr)
-immediate detorsion and orchieoplexy to scrotum req
-twisting of spermatic cord leading to arterial occlusion and venous outflow obstruction
-adolescent male pts
-acute pain swelling and elevated testicle

-infection to epididymis
-in children and elderl 2/2 e. coli
- young males 2/2 chlamydia or gonococcus
- swollen, tender, dysuria, fever, scrotal pain
-r/o TT and awdmin AB therapy
Monitoring a pt with ARF:
1. Daily weights
2. Intake
3. Output
4. BP
5. Watch for infection
A> Causes of hypercalciuria, hyperoxaluria
B> Causes of hypercalciuria
1. increased interstitial absorptin of calcium
2. dec renal reabsorption of calcium, leading to increased renal excretion of Ca2+
3. increase bone reabsorption of Ca2+
4. Primary hyperparaTH
5. Sarcoidosis
6. Malignancy (MM)
7. Vitamin D excess
classical triad of rcc
flank pain
abdominal mass

< 10%
What is hematuria and how might "gross hematuria" be an emergency?
> 3 erythrocytes/HPF on UA
-microscopic more commonly glomeruluar in origin
-gross is more commonly associated with nonglomerular origin
-gross hematuria is common in presention of pts with BLADDER cancer (80%) and RCC in up to 40% of cases
most common findings in patients with ARF?
Weight gain
(2/2 H2O and sodium balance)
Causes of type II RTA?
wilsons dz
lead tox
nephrotic syndrome
When is a renal arteriography ordered?
evaluate for renal artery occlusion - only perform if speific therapy makes difference
most testicular cancers are ____ whereas extratesticular tumors within the scrotum are benign
Courses/phases of ATN
1. Onset
2. Oligouric phase(azotemia, uremia (10-14days); urine output <400 -500mL/day
3. Diuretic phase (urine output >500mL/day) - high urine output 2/2 fluid overload (retained salt, water, other solutes that were retained during oligouric phase)
4. recovery phase - recovery from acute tubular function
How might CRF alter the sexal reproduction function of pateints?
Hypothalamic-pituitary disturbances and gonadal response to sex hormones
1. In men = dec testosterone (gynecomastia)
2. in women = amenorrhea, infertility and elevated PROLACTIN
Rx for obstructed stone:

1. Extracorporeal shock wave LITHOTRIPSY

Most common method is the shock wave lithotripsy
-breaks apart stone; once fragmented will pass spontaneously (best if 5mm-2cm in diameter)

If lithotripsy fails, use percutaneous nephrolithotomy if stones > 2cm
diagnosis of prostate cancer
DRE = carcinoma hard, nodular, irregular
-normal feels like thenar eminence
-cancer feels like a knuckle; once palpable its 60-70% likely to have mets somewhere else
-if abnormal then a TRUS is req regardless of PSA

PSA = not cancer specific but can be increased with massage and needle biopsy, bph, prostatistis and age

TRUS with biopsy = repeat for definite diagnosis; indicated with psa > 10ng/dL; PSA velocity > 75 / year~ with abnormal dre
Why might patients with nephrotic syndrome have increased coaguabiltiy?
Because hepatic synthesis of clotting factors is upregulated 2/2 increased albumin production and 2/2 loss of anticoags in urine.
-increased risk of thromboembolism (DT, Rvein thrombus) PE.
_________ ______ may manifest itself as low back pain in an elderly man with prostate cancer
vertebral mets
Acute interstitial nephritis v Chronic interstitial nephritis
AIN-rapid deterioration in renal funtion and is associated with interstiail eosinophils or lymphocytes

CIN - IN has indolence coure and assoicateions with tubulointerstitial fibrosis and atrophy
Intrinsic rx of renal failure
Once ATN develops:
1. supportive therapy
2. eliminate cause/offending agent
3. if oligouric, trial of loops can help blood flow
life threatening complications in CRF?
1/ hyperkalemia - get ECG; K+ levels can still be increased without a change on ECG
2/ Pulmonary edema secondary to volume overload - look for weight gain

3/infections (pneumonia, sepsis, UTI)
What is the diagnosis of/for colicky flank pain that radiates into groin that has a positive UA for blood (hematuria)
Those with nephrotic syndrome should be tested with/for microalbuminemia. Why?
-albumin excretion 30-300 mg/day

If + perform radioimmunoassay
-most sensitive and specific test
-early sign of DM nephropathy
gold std to diagnise ureteral specific obstuction?
IV urogram
- not in preegnant women
-not in allergic patients to dye
-not in RF pts
Type II RTA Treatment
sodium restriction, inc Na+ reabsorption which inc HCO3- reabsorption in the proximal tubule
Causes of Postrenal FAILURE (ARF)
1. Urethral obstruction 2/2 enlarged prostate - BPH
2. Obstructed solitary kidney
3. Nephrolithiasis
4. Obstructing neoplasm (bladder cervix, prostate)
5. Retroperitoneal fibrosis
6. Ureteral obstruction uncommon cause because must be bilateral to cause renal failure
Glomerulonephritis in endocarditis as a secondary GN disease
1. Immune complex mediated as if that of RF

Treatment of rheumatic fever
Rx infection
seminoma treatment?
inguinal orchiectomy and radiation
Lab findings of inter/intrinsic renal failure (ARF)
Bun:Cr serum
-,20:1 because both BUN and Cr levels still elevated but less urea is reabsorbed
->40mEq with FENa > 2-3% because sodium poorly reabsorbed with decreased urine osmolarity <350 mOsm.kg H20; renal absorptino impaired
Urine osmolarity (<350)
Crur:Crpl = 20:1 --> filtrate cannot be reabsorbed thus excreted
Crur; Crpl
Studies to differentiate prerenal v. intrinsic ARF
Pre-renal Intrinsic
1. UA - hyaline abnormal
2. BUN:Cr (>20:1) <20:1
3. FENa <1% >2-3%
4. Urine Osmo > 500 mOSM 250-300 mOsm
5. urine sodium <20 >40
Hematuria + pyuria in pt with nephrolithiasis:
renal stone + infection
Urinarlysis collection:

1. three steps
a. Visual
b. Dipstick
c. Microscopic
clean catch, midsteam sample aftercleaning urethral meatus (usually adequate for UA and UC)

1. Color, clarity
2. Dipstick reactions
-pH = avg ~6 (4.5-8.0)
-specific gravity = proportional to urine osMo *~1.002 --> 1.035)
-increases with volume dec/dec when volume inc
-Protein = >150 mg/day (proteinuria); >3.5g/day (nephrotic); 50-150 mg/day ( (trace); 1+ = 150-500/day; 2+ 0.5-1.5g /day
a. proteinuria: >150 mg/day
b. nephrotic: >3.5 g/day
c. trace protein: 50-150 mg/day
d. 1+: 150-500 mg/day
e. 2+: .5-1.5g/day
-Glucose - excesive = DM
-Blood = hematuria
-Nitrites = bacteria in urine
-Ketones = DKA, starvation
3. Microscopic eval of sediment
-casts, cells, bacteria, WBC, RBC,
8. Leukocyte esterase = WBC in urine
"Analgesic nephropathy pearls"
FOrm of toxic injury to the kidney 2/2 excessive OTC use of pheactein, acetominphen, NSAIDS, ASA

Results in either: Intersitial nephritis (inflammation of interstitium of nephrons) OR renal papillary necrosis

ULtimately leads to either: ARF or CRF
What is IgA nephropathy aka (____ Dz)
Most common cause of GN is IgA
-"Bergers disease"
-asymptomatic recurrent hematuria with mild proteinuria common
-gross hemaruia post infection/exercise common
-renal function is normalmedangial deposition IgA with C3 on EM

No treatment, steroid therapy can work, good Px with RF
how can we rule out testicular torison from epididymis
toirsion is acute

torsion has no fever
Pre-renal failure (ARF)
Serum BUN/Cr >20:1
Urine mOsm/kg H20 inc >500
Dec urine Na+ <20mEq/L (reabsorbed)
FENa+ <1%
Urine/plasma Cr >40:1
Nonemergent indication for = dialysis

1. Cr and Bun levels are no indications for dialysis
2. Symptoms of uremia:
-lethargy/decreased mental status/encephalopathy
Most common cause of death in patients with ARF?
Infection - 75%
Cardiorespiratory complications
Cystinuria resulting in hexagon-shaped crystals are poorly visualized?
cystine stones
upper tract obstruction causes
-kidney stones
-blood clots
-sloughed papilla
-crystal deposition

-retroperitoneal fibrosis
RTA type I leads to:
Metabolic acidosis without anion gap
urine alkalosis 2/2 decreased H+ excretion
increased susceptibiility to renal stones
---->nephrolithiasis (70-80% kidney stones)

Causes: congenital/MM/nephroTOX/AI = SLE, SS/medullary sponge kidney, analgesicnephro

Treatment: administer bicarb for metabolic acidosis - prevents stones too
administer phosphate salts
MPGN as a 2ndary GN disorder
due to HCV (also HBV, syphilis and lupus)
-associated with cryoglobulin
-poor prognosis)
-RF > 50%

no treatment
Suspect renovascular HTn in which 4 situations:
1. Malignant HTN >220/120 and sudde
2. No prior family hx of HTN and sudden in onset
3. Worsening and sudden
4. The HTN is not responding to standard antihistamines
which hormonally active tumor is associated with precosious puberty in children but gynecomastia in adult males
rare 5% non germ cell tumor : Leydig cell tumor
-usually benign
-if malignant then poor prognosis
What is the different between CRF and CHRONIC RENAL INSUFFICIENCY
CR insufficiency = when a patients renal function is irreverisble compromises but not failed.

Usually patients have a serum Cr 1.5-3.0 mg/dL
Preventative measures v. pharmaceutical measured for nephrolithiasis
1. Dietary - high fluid intake (2L/day) - limit animal protein intake if pt has hyperuricouria (UA stone) and limit Ca2 intake if pt has Ca2+ stones

2. pharmacologic - thiazides (HCTZ) diuretics decrease Ca2+ in urine and decrease the recurrence rates especially in pts with hypercalcuria. ALLOPURINOL is best used and effective in patients with UA stones and prevents elevated UA in urine. Good for pts on chemo
Diagnostic approach in ARF
1. Hx/physical exam
2. duration of renal failure; baseline Cr level provides this information
3. 2nd task to determine whther ARF 2/2 prerenal intra; psotrenal causes
-signs of volume depletion and CHF suggests prerenal
-allergic rxns (rash) suggests AIN and intrinsic etiology
-suprapubic mass, BPH, bladder dysfunction suggests post-renal
4. Med review
When might these be performed:

1. prostate specific antigen PSA which normal is less than four
2. digitsl rectal examination DRE
3. transurethral ultrasonography TRUS
1. if psa greater than 10ng/mL then TRUS indicated regardless of DRE
2. if abnormal DRE, TRUS with biopsy indicated regardless of psa levels
3. if psa < 4 ng/mL and DrE is negative than perform an annual follow up
4. if psa = 4.1 ng/mL and or < 10 ng/dL and DRE negative then controvery as what to do next
Tubulointerstitial diseases: AIN - acute interstitial nephritis
Inflammation of interstitium (that which surrounds GM and tubulues)
-10-15% ARF
-causes = allergic treatment to: penicillin, NSAIDS, diuretics, anticoags, phenytoin, sulfas
-infections = GAS, legionella
-CVD = sarcoidosis
Possible presentaiton of GN disease

1. Isolated hematuria
2. Isolated proteinuria
3. nephritic syndrome (hematuria, HTN, azotemia)
4. neprhotic syndrome (proteinuria, edema, hypoalbumin, hyperlipidemia, hypercoag)

Dx: UA (hematuria and proteinuria)
blood test (RFT)
needle biopsy
How is AKPKD diangnosed? Treatment
Ultrasound is confirmatory- - multiple custs appear on the kidney
#2 CT scan//MRI

1. No curative therapy available
2. drain cysts if symptomatic
3. treat infection with AB
control HTN
Analgesic nephropathy is the most common form of DI-chronic renal failure. Both _____ _______ and ______ _____ nephritis are the most common pathologies that are seen with analgesic nephropathy. Patients with chronic analgesic abuse are likely to also develop:
Papillary necrosis
Tubluointerstitial nephritis

Analgesics include: ASA, naproxen that is seen after ingestion of 2-3 k of the index drug. Will have polyuria and setile pyuria )WBC casts seen)

will also develop: premature aging, atherosclerotic vascular disease, and urinary tract cancer
What is dialysis?
Artificial mechanism by whcih fluid and toxic solutes are removed from cicultaion when kidneys cannot do so sufficiently

process: blood interfaces with an articifial colution resembling human plasma (diasylate). Diffusion of fluids and solutes go across semipermeable membrane
clinical features of nephrolithiasis
renal colic
sudden pain that gradually worsens and becomes severe (patient cannot sit still)
n/v are common
ut obstuction has what clinical features?
renal colic pain = common if acute obstruction ... (kidney stone, papilla) clot
recurrent UTi
Good pastures syndrome as a 2ndary disorder causing GN:
1. Triad for proliferative GN (crescenteric)
c. IgG AntiGBM AB

2. Fever, malsia, RPGN, hemoptysis, cough, SOB

3. Lung DZ b4 renal (days - weeks)
What are the primary causes of renal artery stenosis?
1. Atherosclerosis
-usually elderly males
-(1/3) will occur bilaterally
-smoking and inc cholesterol predisposing factors

2. Fibromuscular dysplasia
-seen in younger females especially
-will be BILATERAL 50% of the time