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Renal and Genitourinary Diseases
Terms in this set (66)
What Cr level marks acute kidney injury? What are the RIFLE criteria of AKI?
Cr inc of 50% or absolute inc of 0.5-1.0
Risk: 1.5x Cr or GFR drop 25% or <0.5mL/kg/hr urine for 6 hours
Injury: 2x, 50%, 12 hours
Failure: 3x, 75%, 24 hours
Loss: Complete loss of kidney fx for 4 weeks
ESRD: Complete loss for 3 months
What are some key diagnostic markers of prerenal kidney injury?
BUN:Cr ratio >20:1 (increased)
FeNa <1 (kidney holds onto Na)
Urine-plasma Cr ratio >40:1 (creatinine not reabsorb)
Hyaline casts on urinalysis
Urine osmolality >500
Clinical signs of hypovolemia
What are some key causes of intrinsic renal failure?
Ischemia (shock, CHF, sepsis, DIC)
Nephrotoxins (aminoglycosides, vanco, NSAIDs, radiocontrast, myoglobinuria, hemoglobinuria, cisplatin, multiple myeloma)
Glomerular disease (ex. Goodpastures, Wegeners)
What are key diagnostic markers of intrinsic renal failure?
BUN:Cr ratio <20
Urine osmolality <350
Urine-plasma Cr ratio <20
What are the most common causes of postrenal kidney injury?
Obstruction of solitary kidney
Note: both ureters must be blocked to cause Cr to rise
What is an appropriate diagnostic process for postrenal kidney injury?
Palpate the bladder
Ultrasound for obstruction/hydronephrosis
Catheter for excess urine volume
What do each of the following urine cast types suggest?
Hyaline: prerenal failure
RBC: glomerular disease
WBC: pyelonephritis, acute interstitial nephritis
Fatty: nephrotic syndrome
Muddy Brown: ATN
What are some major complications of acute kidney injury?
Pulmonary edema from ECF expansion
Hyperkalemia (decreased K excretion)
Metabolic acidosis with increased anion gap
Why can radiocontrast media cause ATN?
It causes spasm of the afferent arteriole.
Prevent with saline hydration.
What are the treatments for prerenal, intrinsic and postrenal kidney injury?
Prerenal: tx underlying d/o, give NS to maintain euvolemia/restore BP, stop ACEi/NSAIDs
Intrinsic: if ATN, supportive tx. If oliguric, furosemide helps inc urine flow to improve fluid balance.
Postrenal: bladder catheter to decompress urinary tract
In all cases, correct the fluid imbalance with goal BP 120-140/80-90
What is the general definition of chronic kidney disease? What are the biggest causes?
GFR <60mL/min or structural/fx abnormalities for at least 3 months
#3 Chronic glomerulonephritis
Plasma Creatinine varies inversely with GFR
What are some major complications of Chronic Kidney Disease?
HTN (from inc Renin/Ang/Aldo from decreased GFR) with CHR
Nausea/vomiting/anorexia (from uremia)
Neuro sxs (uremic seizures, asterixis, restless legs)
Hypocalcemia (lethargy, confusion, tetany)
Normocytic normochromic anemia (erythropoetin deficiency)
Bleeding from platelet dysfx
Hyperphosphatemia w/ hypocalcemia
Decreased testosterone, amenorrhea
Immunosuppression (uremia inhibits cellular, humoral response)
What is the diagnostic approach for chronic kidney disease?
Urinalysis with sediment exam
Cr clearance (GFR estimate)
Small kidneys suggest chronic renal insufficiency, little chance of recovery
What are some common side effects of erythropoietin supplementation in CKD?
Red cell aplasia
What are the three life-threatening complications of CKD?
Hyperkalemia (obtain ECG)
How is chronic kidney disease best managed?
Low protein, low-salt diet
ACEi to dilate efferent arteriole, control BP (but use caution, they can exacerbate hyperkalemia)
Calcium citrate to correct hyperphosphatemia
Erythropoietin for anemia if Hgb <10
Cholestyramine UV light for pruritis
What are the main indications for dialysis?
Metabolic acidosis (pH <7.2)
Coagulopathy from renal failure
Intoxications (methanol, ethylene glycol, lithium, aspirin)
What are some pros and cons to hemodialysis vs peritoneal dialysis?
Hemodialysis: efficient, rapid initiation, but can cause hypotension with rapid fluid shifts and hypo-osmolality
Peritoneal dialysis: patient can do it on their own, but can cause hyperglycemia, hypertriglyceridemia and peritonitis, increased abdominal girth
What is "first-use syndrome" in regards to hemodialysis?
Chest and back pain with possible anaphylaxis.
Hemodialysis can also cause amyloidosis of B2 microglolulin in bones and joints
What are the three key features of nephrotic syndrome?
(hypercoag state due to loss of anticoagulants in urine)
What is the diagnostic approach to proteinuria?
Urine dipstick test (specific for albumin, can miss immunoglobulins in multiple myeloma)
Check for microalbuminuria
How is proteinuria treated?
Tx the underlying disease
ACEi (decrease urinary albumin loss)
Diuretics if edema
Limit dietary protein/sodium
Vaccinate vs influenza and pneumococcus
What do microscopic and gross hematuria respectively indicate?
Microscopic: glomerular pathology
Gross: bladder cancer, renal cell carcinoma (requires upper urinary tract CT or IV pyelogram)
What are some major causes of hematuria?
Infection (UTI, urethritis, pyelo)
Glomerular disease, IgA nephropathy
Sickle Cell disease
Meds (cyclophosphamide, anticoag, salicylates, sulfonamides)
What would rhabdomyolysis look like on urinalysis?
Blood on urinalysis in the absence of RBCs on microscopy
In the setting of hematuria, what do RBC casts and proteinuria on urinalysis indicate?
Glomerulonephritis or another glomerular cause
What are some key differences between glomerular and tubular diseases?
Glomerular: chronic, not caused by toxins, causes nephrotic syndrome, often requires biopsy, tx with steroids or immunosuppressants
Tubular: acute, due to toxins, doesn't require biopsy
Minimal Change Disease
Nephrotic syndrome most common in children and ~lymphoma
No light microscope histologic abnormalities
Fusion of glomerular foot processes on electron microscopy
Likely due to T-cell dysfunction
Responsive to steroid therapy
Focal Segmental Glomerulosclerosis (FSGS)
Nephrotic, often with hematuria and HTN
Resistant to steroid therapy
Tx: cytotoxic agents, steroids, immunosuppression, ACEi/ARB
Nephrotic with thickened glomerular capillary walls
Idiopathic or due to infection (hepatitis, syphilis, malaria) or drugs (gold, captopril, penicillamine), neoplasm or lupus
Asymptomatic except after URI or exercise (gross hematuria)
#1 cause of glomerular hematuria
Mesangial IgA and C3 on electron microscopy
Alport Syndrome (hereditary nephritis)
X-linked or auto dom
Hematuria, pyuria, proteinuria
High-frequency hearing loss w/o deafness
Progressive renal failure
No tx :(
Persistent activation of alternative complement pathway
Often from Hep C infection, syphilis, lupus
Poor prognosis, with renal failure in 50%
#1 cause of nephritic syndrome
10-14 days after a strep infection of URI or skin
More in kids
Hematuria, low complement, HTN, proteinuria
Self-limited with supportive therapy
Proliferative GN (crescentic)
IgG anti-glomerular basement membrane Ab
Lung disease precedes renal
Renal biopsy: linear immunofluorescence pattern
Tx: plasmapheresis, cyclophosphamide, steroids
What is the most common cause, presentation and dx/tx for acute interstitial nephritis?
Acute allergic rxn to medication is #1 cause. Others include Strep or legionella infection, collagen vascular d/o, SLE, sjogren's.
Sxs: AKI with rash, fever, eosinophilia
Dx: increased BUN and Cr, eosinophiluria
Tx: remove offending agent, steroids
What are the characteristic findings in chronic vs acute interstitial nephritis?
Chronic: Tubulointerstitial fibrosis and atrophy
Acute: interstitial eosinophils and lymphocytes
What is the general pathology of renal tubular acidosis and what are the three types?
Non-anion gap hyperchloremic metabolic acidosis
Glomerular function preserved
Describe the pathophysiology, sxs and treatment for type 1 (distal) renal tubular acidosis.
Inability to secrete H in the distal tubule, so cannot acidify urine below pH=6 and cannot generate bicarbonate.
Increased excretion of ions --> hypokalemia, decreased ECF volume
Renal stones and nephrocalcinosis are very common
Tx: sodium bicarconate and phosphate salts
Describe the pathophysiology, sxs and treatment for type 2 (proximal) renal tubular acidosis.
Inability to reabsorb HCO3- at proximal tubule.
Hypokalemia without renal stones.
~Fanconi's syndrome, Wilson's disease, cystinosis, lead toxicity, multiple myeloma, amyloidosis
Tx: sodium restriction (increases reabsorption of everything in the prox tubule)
Describe the pathophysiology, sxs and treatment for type 4 renal tubular acidosis.
From any condition leading to hypoaldosteronism
Decreased Na absorption
Decreased K and H secretion in the distal tubule
Hyperkalemia and acidic urine
What is the pathophysiology, sxs and tx for Hartnup disease?
Defective amino acid transporter (auto rec)
Decreased intestinal/renal absorption of neutral amino acids leading to nicotinamide deficiency
Sxs: like pellagra (dermatitis, diarrhea, ataxia, psych)
Tx: supplemental nicotinamide
What is the pathophysiology, sxs and treatment for Fanconi's syndrome?
Proximal tubule dysfx leading to defective transport of glucose, aa, Na, K, Ph, uric acid, bicarb
Sxs: glucosuria, phosphaturia with skeletal problems, proteinuria, dehydration, polyuria, hypercalciuria, hypokalemia
Tx: phosphate, K, alkali, salt supplements
What are the clinical features of ADPKD, and how is it dx and tx?
Dx: ultrasound (multiple cysts)
Tx: no curative therapy but can drain cysts if needed
What are the key symptoms of autosomal recessive polycystic kidney disease? How is it dx and tx?
Cysts in the renal collecting ducts and hepatic fibrosis!
Kidneys increased in size, pulmonary insufficiency from hypoplasia, HTN
Oligohydramnios as a fetus
Tx: none. manage newborn respiratory issues. renal replacement tx in ESRD.
What is the most common symptom of renal artery stenosis? What are the two biggest causes and how is it dx/tx?
Sxs: Secondary HTN (can be quite severe), abdominal bruit
Causes: Atherosclerosis, fibromuscular dysplasia
Dx: Renal arteriogram (nephrotoxic, don't use in ESRD)
MRA (magnetic is OK for ESRD)
Tx: Revascularization with percutaneous transluminal renal angioplasty
What is the underlying cause of hypertensive nephrosclerosis? How do benign and malignant nephrosclerosis differ in presentation?
Cause: systemic HTN increases capillary hydrostatic pressure in glomeruli, causing sclerosis
Benign: mild/moderate increase in Cr, microscopic hematuria, mild proteinuria
Malignant: rapid increase in Cr, RBC/WBC casts, nephrotic syndrome, papilledema, CNS findings. More in AA men.
What portion of the kidney is most commonly affected in sickle cell nephropathy?
Can lead to necrosis, renal failure, nephrotic syndrome and UTIs
What are the most common sites of nephrolithiasis, and what are some risk factors?
Calyx of kidney
Low fluid intake (#1)
Gout, type 1 RTA
Low calcium/high oxalate diet
What are the four main types of kidney stones? What does each look like on x-ray and what are the main causes of each?
Calcium (#1): radiodense, bipyramidal, from hypercalcemia or hyperoxaluria
Uric Acid: radiolucent, flat/square plates, from hyperuricema (~chemo, gout)
Struvite: radiodense, rectangular prism, from urease-producing bacteria in UTI (Proteus, Klebsiella, Serratia, Enterobacter), facilitated by alkaline urine
Cystine: hexagon crystals
What is the classic presentation of a kidney stone? How is it best dx?
Renal colic with hematuria. Sometimes nausea/vomiting
Urinalysis shows hematuria with sediment crystals. Urine culture if suspect infection. KUB (cystine and uric acid stones won't show).
Spiral CT w/o contrast is gold standard! Shows all stones.
Ultrasound in pregnant women
How is nephrolithiasis best treated?
Hydration with >2L fluids/day
If stone <0.5cm, outpatient tx.
If >0.5 and <2cm, extracorporeal shock wave lithotripsy
If >2cm, percutaneous nephrolithotomy
Prevention: high fluid, low protein/calcium.
Thiazides reduce urinary calcium
Allopurinol reduces uric acid levels in urine
What are the main complications of urinary tract obstruction, and how are upper and lower obstructions differentiated?
Can cause renal insufficiency and hydronephrosis
Upper: above ureterovesicular junction, causes renal colic.
Lower: below junction, affects urination. ~BPH, prostate cancer, neurogenic bladder, bladder cancer
What is the classic diagnostic approach to urinary tract obstruction? How are upper and lower obstructions treated, respectively?
Dx: renal ultrasound (shows dilation) is most sens/spec. Urinalysis. IV urogram (IVP) is gold standard for ureteral obstruction.
Lower: urethral catheter, dilatation, prostatectomy
Upper: nephrostomy tube, ureteral stent
If acute obstruction UTI, immediate US and intervention.
What type of cancer are most prostate cancers? What are the main clinical features of it?
Cancer begins in periphery of gland and moves centrally. Often has metastasized to bone (vertebral bodies, pelvis) or lymph nodes before detection.
How is prostate cancer best diagnosed?
DRE: hard, nodular, irregular feel (if palpable, 60-70% have spread beyond prostate)
PSA: not a screening test, but levels correlate with prostate volume
Transrectal ultrasound: if DRE is abnormal or PSA >10
How is prostate cancer treated depending on the extent of its spread?
Localized to prostate: radical prostatectomy (se: ED, urinary incontinence)
Locally invasive: radiation therapy androgen deprivation
Metastatic: reduce testosterone amount via orchiectomy, antiandrogens, GnRH antagonists, and LH-blockers
What are some risk factors for RCC, and how does it present? Dx/tx?
Risks: smoking! chronic dialysis, ADPKD, HTN
Sxs: hematuria flank pain flank/abd mass
Dx: renal ultrasound --> abdominal CT
Tx: radical nephrectomy (remove kidney and adrenal gland)
What are some paraneoplastic syndromes associated with RCC?
Polycythemia (from erythropoietin)
Hypercalcemia (from PTH-like hormone)
HTN (from renin)
Cushing's syndrome (from cortisol)
Feminization/masculinization (from gonadotropins)
What type of cancer are most bladder cancers? What are risks, sxs? Dx/tx?
Transitional Cell Carcinomas
Risks: smoking, aniline dyes, azo dyes
Sxs: painless hematuria, possible dysuria
Dx: urinalysis/urine culture, urine cytology, cystoscopy with biopsy (definitive)
Tx: depends on stage, tends to recur
What are the two categories of germ cell testicular cancers, and what are the key characteristics of each?
Seminomas: most common, slow growth, late invasion
1. Embryonal: ~malignant, hemorrhage, necrosis, mets to lymph/lungs
2. Choriocarcinoma: high hCG, aggressive, mets early
3. Teratoma: high AFP, hCG, rare mets
4. Yolk sac: high AFP, more in young boys
What are the non-Germ cell tumors of the testicles?
Leydig Cell: benign but hormonally active, present with gynecomastia or precocious puberty
Sertoli Cell: benign
How is a testicular cancer best diagnosed?
Testicular mass on exam
US of testicles
B-hCG: elevated in choriocarcinoma
AFP: elevated in embryonal (never in chorio or seminoma)
CT for staging
In what population is penile cancer most common, and what are some risk or protective factors?
Men in seventh decade
RIsks: HSV, HPV-18
How does testicular torsion present, and how is it treated?
Sxs: acute severe testicular pain, swollen/tender scrotum, elevated testicle
Tx: surgery within 6 hours to prevent infarction. Typically perform bilaterally.
How is the presentation of epididymitis different from testicular torsion? What organism most commonly causes epididymitis?
Epididymitis presents with fever, which torsion doesn't. Otherwise, sxs are similar.
~E coli and gonorrhea/chlamydia if sexually active
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