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Urology/Nephrology

Urology/Nephrology. Lecture Five—March 4, 2013. Acute Renal Failure. Acute Renal Failure . “Acute Kidney Injury” Sudden decrease in renal function  inability to maintain acid-base balance Inability to maintain fluid balance Inability to maintain electrolyte balance

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Urology/Nephrology

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  1. Urology/Nephrology Lecture Five—March 4, 2013

  2. Acute Renal Failure

  3. Acute Renal Failure • “Acute Kidney Injury” • Sudden decrease in renal function • inability to maintain acid-base balance • Inability to maintain fluid balance • Inability to maintain electrolyte balance • Inability to excrete nitrogenous wastes • Serum Creatinine is a convenient marker

  4. Acute Renal Failure • RIFLE Criteria—3 progressive levels of acute kidney injury based on elevation in serum Cr or decline in urinary output with two outcome measures (loss and ESRD) • Risk—1.5-fold increase in serum Cr or urine output < 0.5 mL/kg/h × 6 h • Injury—2-fold increase in serum Cr or urine output < 0.5 mL/kg/h x 12 h • Failure—3-fold increase in serum Cr or urine output <0.5 mL/kg/h x 24 h • AKIN Criteria—similar, also mention serum Cr >0.3 mg/day is risk for acute kidney injury • Serum Cr increases 1-1.5 mg/dL if no renal function • 5% of hospital admissions and 30% of ICU admissions have a diagnosis of acute kidney injury/acute renal failure • ARF will develop in 25% of hospitalized patients • ARF of any typehigher risk for all-cause mortality

  5. Acute Renal Failure—Signs/Symptoms • Nonspecific • Often due uremia or underlying cause • Uremia—N/V, malaise, altered sensorium • Hypertension • Hypovolemia or hypervolemia • Hypervolemiarales • Pericardial effusions/friction rub • Cardiac tamponade • Arrhythmias (hyperkalemia) • Abdominal pain and ileus • Bleeding and clotting disorders • Encephalopathy and seizures

  6. Acute Renal Failure—Labs • Elevated BUN/Cr • Hyperkalemia • impaired K+ excretion • ECG—peaked T waves, long PR, wide QRS, long QT if hypocalcemia is also present • Metabolic Acidosis • decreased organic and nonorganic acid clearance • Hyperphosphatemia • impaired phosphate excretion • Anemia • decreased erythropoetin production • platelet dysfunction

  7. Acute Renal Failure—Prerenal • Most common reason for ARF (40-80%) • Prerenal azotemia – due to renal hypoperfusion • Decreased intravascular volume • Changes in vascular resistance • Low cardiac output—low effective renal arterial flow • BUN:Cr ratio typically >20:1 (increased urea reabsorption) • Low fractional excretion percent of sodium • High urine osmolality • Urinary sediment—benign or hyaline casts • Treatment—CORRECTION OF UNDERLYING CAUSE • Maintain euvolemia • Maintain normal K+ levels • Avoid nephrotoxic drugs

  8. Acute Renal Failure—Postrenal • Least common reason for ARF (5-10%); Reversible • Post renal azotemia—urinary flow from both kidneys (or a single functional kidney) is obstructed • Elevated intraluminal pressure  parenchymal damage • Urethral obstruction, bladder dysfunction or obstruction, obstruction of both ureters or renal pelvises • Initially—high urine osmolality, low urine sodium, high BUN:Cr (>20:1)—similar to prerenal ARF • After several days—low urine sodium, low osmolality • Treatment—CORRECTION OF UNDERLYING CAUSE • Avoid post-treatment volume depletion • Prompt treatment can result in partial or complete reversal

  9. Acute Renal Failure—Hydronephrosis

  10. Acute Renal Failure—Intrinsic • Up to 50% of all cases of ARF • Exclude prerenal and postrenal causes of ARF • Major injury sites—tubules, interstitium, vasculature, glomeruli • Acute Tubular Necrosis—ischemia, nephrotoxins • Acute Glomerulonephritis—immune complex-mediated, pauci-immune, anti-GBM • Acute Interstitial Nephritis—allergic reaction, drug reaction, infection, collagen vascular disease

  11. ARF—Acute Tubular Necrosis • 85% of intrinsic acute renal failure • Ischemia—tubular damage from states of low perfusion • Inadequate GFR and inadequate blood flow to maintain parenchymal cellular formation • Nephrotoxins—exogenous more commonly cause damage than endogenous • Exogenous—aminoglycosides, amphotericin B, vancomycin, acycovir, cephalosporins, radiographic contrast media, cycosporine, antineoplastics, mercury, cadmium, arsenic • Endogenous—heme-containing products, uric acid, paraproteins

  12. Exogenous Nephrotoxins • Aminoglycosides—up to 25% on therapeutic levels; medication can remain in renal tissues for up to 1 month • Amphotericin B—can cause hypokalemia and nephrogenic diabetes insipidus • Radiographic contrast media—contrast nephropathy is 3rd leading cause of new ARF in hospitalized pts • Combination of DM and kidney dysfunction poses greatest risk • Can reduce risk by using less contrast and IV infusion of NS before and after contrast • Others—vancomycin, IV acyclovir, cephalosporins, cyclosporine, antineoplastics, heavy metals

  13. Endogenous Nephrotoxins • Myogobinuria—from rhabdomyolysis • mainly when CK >20,000-50,000 • False + urine dip for hemoglobin (dark brown but NO RBCs) • ↑ K+, Phosphate, uric acid; ↓ Calcium • Volume repletion • Hemoglobin—hemolysis • Hyperuricemia—cell lysis • Bence Jones Protein—seen with multiple myeloma Dark urine in Rhabdomyolysis Bence Jones protein

  14. ARF—Acute Tubular Necrosis • Signs/Symptoms—see general ARF S/S • Labs—BUN:Cr < 20:1 (tubular function not intact) • ↑ K+, phosphate, urine Na • may see brown urine • +/- oliguria • Pigmented granular casts or “muddy brown casts” • Renal tubular epithelial cells or epithelial cell casts

  15. ARF—Acute Tubular Necrosis 1. Bland sediment2. Renal tubular epithelial cells3. Renal tubular epithelial cell cast4. Finely granular casts 5. Muddy brown casts with necrotic debris Muddy brown cast in ATN

  16. ARF—Acute Tubular Necrosis • Treatment—avoid volume overload and hyperkalemia • Loop diuretics—often used at high doses; controversial • Restrict dietary protein to 0.6 g/kg/d to prevent metabolic acidosis • Improve ↑ Ca and phosphate with diet and phosphate-binding agents; • Dialysis—if life-threatening electrolyte disturbances, volume overload unresponsive to diuresis, worsening acidosis, or uremic complications • Prognosis—initial injury, maintenance, and recovery • maintenance phase—1-3 weeks—cellular repair and removal of tubular debris • recovery phase—GFR begins to rise and BUN/Cr begin to fall • Mortality—20-50% in hospitalized settings, can be up to 70% • Leading causes of death—infections, fluid/electrolyte imbalance, worsening of underlying disease

  17. ARF—Interstitial Nephritis • 10-15% of intrinsic ARF; 70% of cases 2o drugs • Other causes—infections, immunologic disorders, idiopathic • Interstitial inflammatory response with edema and possible tubular cell damage • Signs/Symptoms—fever (>80%), transient maculopapular rash (25-50%), eosinophilia (80%) • Urine—RBCs (95%), WBCs, WBC casts, eosinophils • Treatment—removal of cause; supportive; steroids • Recovery in weeks-months • May need urgent dialysis for up to 1/3 of pts • Often good prognosis; rarely progress to ESRD

  18. ARF—Glomerulonephritis • Rare—5% of ARF; inflammatory glomerular lesions on pathology • Immune complex deposition—IgA nephropathy (Berger disease), post-infectious glomerulonephritis, endocarditis, lupus nephritis, cryoglobulinemic, MPGN • Anti-GBM—confined to kidney or associated with pulmonary hemorrhage; autoantibodies against GBM • Pauci-immune—small vessel vasculitis associated with ANCAs (granulomatosis with polyangiitis/Wegener granulomatosis) • Other causes—HTN emergencies, Hemolytic-uremic syndrome, Thrombotic thrombocytopenic purpura

  19. ARF—Glomerulonephritis • Signs/Symptoms—hypertensive, edematous • Labs—elevated BUN/Cr (usually >20:1 ratio)—not reliable marker of kidney function • Urine—hematuria, proteinuria (<3 g/d), RBCs, RBC casts, WBCs • Other tests—complement, ASO, anti-GBM, ANCAs, ANA, hepatitis panel, blood culture, renal US, renal bx • Treatment—depends on underlying cause • steroids, cytotoxic agents • plasma exchange if Goodpasture disease or pauci-immune

  20. Chronic Kidney Disease

  21. Chronic Kidney Disease • > 20 million Americans • 1 in 9 adults • Over 70% of stage 5 CKD and ESRD—DM or HTN • Rarely reversible—progressive decline in function even after the inciting event is removed • Independent risk factor for cardiovascular disease • Read – Table 22-5 p. 884—stages of CKD

  22. Chronic Kidney Disease • Signs/Symptoms—asymptomatic for most of course • S/S manifest usually when CKD well advanced ( GFR <10-15) • Build up of metabolic waste/uremic toxins  uremic syndrome (Table 22-7) • Most common physical finding—HTN • Other findings—sallow skin, easy bruising, uremic fetor, cardiopulmonary signs, altered mental status • S/S of uremia—immediate admission and nephro consult • ID and correct reversible causes or exacerbating factors • Imaging—small echogenic kidneys bilaterally supports dx • Labs—documented ↑ BUN/Cr over at least 3 mo, or persistent proteinuria or abnormal renal imaging (even if GFR is normal) • Urine sediment—broad, waxy casts may be present • Proteinuria—if present, quantify

  23. CKD—Cardiovascular Complicatons • Death from CV disease—45% of all pts on dialysis • 80-90% of CKD pts die before reaching need for dialysis • HTN—most common complication of CKD • Nonpharmacologic therapy—decrease salt intake to 3 g/d (2g/d if persistent HTN or CHF); weight loss; exercise; treat OSA • Pharmacologic therapy—diuretics; ACE/ARB (Monitor Cr and K+) • Second line drugs—CCBs, BBs; often need adjunct drugs • Goal of <130/80 mmHg • CAD—aggressively treat risk factors • CHF—fluid and salt restriction; diuretics; ACE • Pericarditis—rare—uremic pericarditis  mandatory hospitalization and hemodialysis

  24. CKD—Mineral Metabolism • Typical: ↑ phosphate, ↓ Ca and vit D, secondary hyperparathyroidism due to first 3 abnormalities • Increased fracture risk; now also noted increased vascular calcification • Renal Osteodystrophy—common—includes osteitisfibrosacystica; metastatic calcifications; adyamic bone disease; osteomalacia • Bone pain, proximal muscle weakness, higher risk for fractures • Correct calcium, phosphorus, and vitamin D levels as well as hyperparathyroidism • Dietary phosphorus restriction, phosphorus binders, vitamin D replacement therapy

  25. CKD—Hematologic Complications • Anemia—mainly due to decreased erythropoetin • Erythropoetin-like agents approved for goal Hgb of 10-12 if no other treatable causes of anemia present • Higher Hgb—increased risk of stroke and other CV events • HTN—complication of erythropoietin or darbepoetin in 20% • Iron deficiency—impaired GI iron absorption • Ferritin <100-200 or iron saturation <20% is abnormal • Check iron studies, thyroid, vitamin B12, folate and fecal occult blood before starting erythropoetin • Coagulopathy—platelet dysfunction • Treatment—only if symptomatic • Raising Hgb to 9-10 • Desmopressin—short-lived but effective (surgery) • Conjugated estrogens—can help for several weeks but rarely used • Dialysis—improves beeding time but does not normalize • Cryoprecipitate—lasts <24 hrs—rarely used

  26. CKD—Other Complications • Hyperkalemia—CKD stages 4-5 but can occur earlier • cardiac monitoring if EKG changes or >6.0-6.5 mEq/L • sodium polystyrene sulfonate; β-agonists, insulin + glucose, calcium gluconate • Chronically elevated K+ - dietary K+ restriction (2 g/d), adjust medications, loop diuretics • Acid-Base Disorders—inability to excrete acid from dietary proteins • mainly due to loss of renal mass • treat with sodium bicarbonate • Neurologic Complications— • uremic encephalopathy (GFR <5-10)—improves with dialysis • neuropathy—65% of stage 5 and ESRD pts—varied presentations • Endocrine Complications— • Diabetics—higher circulating insulin levels; may need to adjust meds • discontinue metformin if GFR <60 due to increased risk of lactic acidosis • Sexual dysfunction—decreased testosterone and anovulation • faster progression of CKD during pregnancy if Cr >1.4 • Infertility common and pregnancies often have poor outcomes • renal transplant is best option for ESRD pts wishing to have children

  27. CKD—Dietary Management • Protein Restriction—may slow progression to ESRD but low serum albumin at dialysis initiation is a strong predictor of mortality • Salt and Water Restriction—2 g/d sodium; 2 L/d of fluid • Potassium Restriction—GFR <10-20 or once pt becomes hyperkalemic; <50-60 mEq/d • Phosphorus Restriction–dietary intake 800-1000 mg/d • below GFR 20-30, phosphorus binders usually needed • Magnesium Restriction—dangerously high levels rare unless received in medication or IV

  28. CKD—Dialysis • GFR 10 mL/min or Cr 8 mg/dL(GFR 15 mL/min / Cr 6 mg/dL in DM) • Other indications—uremic symptoms, fluid overload unresponsive to diuresis, refractory hyperkalemia, severe metabolic acidosis (pH <7.2) • Hemodialysis—semipermeable membrane with constant flow of blood along one side and diasylate on the other • usually 3 sessions/wk, 3-5 hrs each • Peritoneal dialysis—diasylate instilled into peritoneal cavity and exchanged periodically • improved autonomy • minimizes symptomatic volume and electrolyte shifts • less dietary restrictions • lower overall cost • preferred by patients • Cons – removes large amounts of albumin, peritonitis is a risk

  29. CKD—Kidney Transplant • Up to 50% of all pts with ESRD are suitable for transplant • 2/3 from deceased donors, 1/3 from living donors • 1-yr survival—95% (living), 89% (deceased) • 3-yr survival—88% (living), 78% (deceased) • Immunosuppressive regimens required • Higher risk for certain cancers and infections

  30. CKD—Prognosis • Mortality higher in dialysis than transplant patients • Overall 5-year survival for CKD pts—36% • Average life expectancy for dialysis pts—3-5 yrs • Most common cause of death—cardiac disease (45%) • infection (14%), cerebrovascular disease (6%), cancer (4%) • Mortality predictors—DM, advanced age, low albumin, low socioeconomic status, inadequate dialysis • ESRD without dialysis—death in days-weeks • Uremia, arrhythmias, volume overload, dyspnea

  31. Questions?

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