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Acute Renal Failure
Karen L.Herbst MD PhD University of Washington

Functional Classification of Acute Renal Failure (ARF)
• •

Hemodynamic ARF (≈30%) Parenchymal ARF (65%)
• • • • Acute tubular necrosis (55%) Acute glomerulonephritis (≈5%) Vasculopathy (3%) Acute interstitial nephritis (≈2%)

•

Obstruction (≈5%)

Differentiating ARF vs. Chronic Renal Failure (CRF)
1) 2) 3)History Oliguria = ARF; acute CRF decompensation Renal ultrasound
• • Normal or large = acute CRF – small (unless PKD, diabetes, amyloid)

4) 5) 6) 7)

ARF =Unstable azotemia (↑ or ↓ over days) Anemia – unreliable for ARF vs. CRF ↑PO4, ↑K+, metabolic acidosis, ↑uric acid – little diagnostic value Urinalysis – no value unless normal suggesting pre-renal azotemia

Pre-Renal AzotemiaDefinition: A reduction in glomerular filtration rate (GFR) due to a ↓ glomerular capillary pressure Diagnosis: Characteristic clinical setting and urinary findings Response to the correction of the presumptive pre-renal state

Pre-Renal Azotemia: Causes
1)

↓ cardiac output
• • CHF Intravascular volume depletion

2)

Normal Cardiac Output
• • • Selective renal vasoconstriction (NSAIDS, ↑Ca++)ACE (-) in patients with pre-existent renal vascular disease Hepatorenal syndrome

3)

↑ cardiac output
• • Hepatorenal syndrome Sepsis syndrome

Pre-Renal Azotemia: Renal Manifestations
1) 2) 3) 4) 5)

Na+ avidity Relatively normal urinalysis Relatively normal serum bicarbonate High BUN/creatinine ratio (not always) High urine osmolality (typically >600 mosm/kg)

Pre-Renal Azotemia:Confounding Diagnostic Variables
1)

A low urine Na+ is not unique – Found in:
• • • Non-oliguric ATN, especially contrast-induced Early urinary tract obstruction Acute glomerulonephritis

2) 3) 4)

Diuretic use can obfuscate the urine Na+ and urine osmolality Jaundice – muddy brown granular casts Poor dietary intake lowers the BUN/Cr ratio

Hepatorenal Syndrome (HRS)
Definition:“Irreversible” pre-renal azotemia in the setting of end-stage hepatic disease Pathogenesis: 1) Unrelenting renal vasoconstriction induced by unknown mediators 2) Renin/angiotensis, endothelin, NO, prostanoids, endotoxin, ↑sympathetic tone all implicated; none proven and may reflect secondary phenomena

HRS: Differential Diagnosis
Rule out volume depletion by volume challenge 2) Rule out combinedhepatic and renal epithelial injury 3) Rule out ATN (which is common in the HRS patients)
1)

HRS: Therapy
1) 2) 3) 4)

Portal-systemic shunts: acute, but not longterm benefits Paracentesis: no proven benefit; may precipitate ARF Vasodilator therapy: no proven benefit Dialysis:
• • IF a possibility of hepatic functional recovery IF there is a likelihood of ATN (high urine Na+; urine sedimentnot helpful)

5)

Hepatic transplantation

Obstructive Nephropathy
1) 2)

Incidence: ≈ 5-10% ARF cases Causes: in part segregates according to age: • Children: anatomic (urethral valves, ureteral-vesicle or ureteral-pelvic stenoses) • Young adults: stones; retroperitoneal processes (tumor, infections) • Elderly: GU tumors (bladder, cervical); BPH

Obstructive Nephropathy
3) • • • •4)

Pathogenesis: Acute ↑ in intraluminal pressure 2° renal vasoconstriction (TXAII) “Disuse atrophy” Inflammatory cell mediated tubulointerstitial injury Symptoms:
• • Pain (> common if acute; ↑ with solute load Abnormal urine flow – absolute anuria (R/O acute GN, cortical necrosis), oliguria, or nonoliguria Hematuria

•

Urinary Tract Obstruction Diagnosis
History: most often suggeststhe diagnosis
1)

2)

Urinalysis • RBCs, minimal proteinuria, pyuria, bacteriuria • Urine Na+: low (early); high (late) Foley catheter (excludes only bladder outlet obstruction

Urinary Tract Obstruction Diagnosis
3)

Renal Ultrasound (95% accurate) Possible false negatives:
• • • • • Early obstruction ( 12 weeks; but highly variable) Coincidental diseases (e.g., UTI)

4)

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