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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

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