Renal Pathophysiology

CHAPTER 11 Acute Kidney Injury

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TABLE 11.1. Major Causes of Acute Renal Injury I. Prerenal disease A. Volume depletion due to gastrointestinal, renal, or third-space losses D. Bilateral renal artery stenosis, particularly after the administration of a renin-angiotensin system inhibitor (angiotensin-converting en zyme inhibitor [ACEi] or angiotensin receptor blocker [ARB]) E. Drugs that interfere with autoregulation such as nonsteroidal an ti-inflammatory drugs (NSAIDs) F. Shock due to fluid loss, sepsis, or cardiac failure—frequently pro gresses to acute tubular necrosis II. Intrinsic renal disease A. Glomerular disease 1. Acute glomerulonephritis, including postinfectious glomerulone phritis and lupus nephritis 2. Crescentic or rapidly progressive glomerulonephritis 3. Microangiopathic hemolytic anemias including hemolytic-uremic syndrome and thrombotic thrombocytopenic purpura B. Tubulointerstitial disease 1. Acute tubular necrosis B. Congestive heart failure or valvular heart disease C. Hepatorenal syndrome with hepatic cirrhosis A. Postischemic—following any cause of severe renal ischemia B. Toxic—drugs such as aminoglycoside antibiotics and chemo therapy agents such as cisplatinum, radiocontrast agents, or the excretion of heme pigments with hemolysis or rhabdomyolysis 2. Interstitial nephritis, acute, usually drug induced 3. Intratubular obstruction, due to immunoglobulin light chains in multiple myeloma, drugs such as the antiviral drug acyclovir, or uric acid crystals following excess tissue breakdown and release of purines after chemotherapy or radiation therapy of a hematologic malignancy (tumor lysis syndrome) C. Vascular disease 1. Vasculitis, usually associated with systemic symptoms 2. Atheroemboli to the kidney, most often following surgical or ra diologic procedures with manipulation of an atheromatous aorta renal injury was sustained in the preceding 24 hours (such as an episode of hypotension, the institution of therapy with an angiotensin-converting en zyme [ACE] inhibitor or a nonsteroidal anti-inflammatory drug [NSAID], or the administration of a radiocontrast agent) or the cumulative effect of a toxin became clinically apparent (such as acute tubular necrosis [ATN] due to an aminoglycoside antibiotic). Recall that GFR estimates from the serum creatinine reflect total function, so processes affecting a single kidney (stone, ischemia) may not manifest a noticeable elevation in creatinine concentration. Although GFR estimates from a rising creatinine in the acute setting reflect AKI, the actual GFR cannot be estimated until a new steady state is achieved. III. Urinary tract obstruction A. Prostatic disease in men B. Pelvic or retroperitoneal malignancy

CHAPTER 11 Acute Kidney Injury

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