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01-09-2010 | Nephrology in Brief
Nephrology in Brief 19:5
Published in: Kidney | Issue 5/2010
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ACUTE RENAL INJURY (AKI)-
Regulatory T cells (Treg) are anti-inflammatory lymphocytes that inhibit the function of pro-inflammatory neutrophils and macrophages and protect the kidney against ischemic injury. This maybe achieved experimentally by causing them to accumulate following repeated exposure to short periods of ischemia (“preconditioning” ) or by increasing their number in the kidney (“adoptive transfer”). Conversely, pretreating animals with Treg depleting antibody results in more severe ischemic damage (Kid Int 77:771).
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Markers of tubular injury used to identify early AKI and provide prognostic information have included serum albumin, α1- microglobulin, β2- glycoprotein, plasma retinol-binding protein, NHE3, N-acetyl-glucosamidase, neutrophil gelatinase-associated lipocalin (NGAL), cytokines, proteases, and kidney injury molecule-1 (KIM-1). More recently two spots identified by proteonomic methods as containing albumin and plasma retinol-binding protein have been claimed to distinguish acute tubular necrosis from prerenal azotemia in 90% of cases (J Investig Med 58:612).
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A meta-analysis of 19 studies found NGAL to be an early predictor of acute tubular necrosis, equally useful at a cut-off concentration >150 ng/ml in urine or plasma, and having prognostic value for outcomes such as dialysis and death (Am J Kidney Dis 54:987 and 1,012).
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By contrast, a study of 451 critically injured adults found that a single measurement of urinary NGAL had only moderate utility in predicting the development and severity of AKI. Its additional contribution to conventional clinical risk predictors was limited (J Am Soc Nephrol 20:1,823).
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Also of limited value in AKI were cystatin C levels, no better than serum creatinine, BUN, and urine output in predicting the need for dialysis or eventual death. Cystatin C is an enzyme synthesized by all nucleated cells, freely filtered by the glomerulus, and metabolized completely by the proximal tubule. Its levels maybe influenced by markers of inflammation (white cell count and C-reactive protein) and also by insulin, cortisol, and thyroxin (Am J Kidney Dis 54:1,025).
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More useful, though all too often neglected, was urine microscopy. In a scoring system based on the number of renal tubular epithelial cells and casts, it predicted developing acute tubular necrosis, worsening renal failure, dialysis, or death (Clin J Am Soc Nephrol 4:1,914).
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US veterans surviving an episode of AKI for at least 90 days and not requiring dialysis had a 41% higher than expected mortality within the next 2 years. The risk increased with the severity of the AKI, possibly because of lower residual “kidney reserve”, injury to other organs during the AKI episode, or comorbidities not detected in the study (J Am Soc Nephrol 21: 345).
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Patients with underlying renal disease developing AKI in an intensive care units had a lower mortality than if they started off with normal renal function, possibly because they had a less severe illness. They were however 1 ½ times more likely to become dialysis dependent than if they had normal renal function (Clin J Am Soc Nephrol 4:1,914).
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In a study of 963,730 admissions, patients admitted with AKI on a weekend were more likely to die and less likely to receive dialysis than those admitted on a weekday. The risk of dying was increased 22% by day 3 of admission and 7% during the entire hospital stay (J Am Soc Nephrol 21:845).
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A patient presenting with AKI (serum creatinine 6 mg/dl), two past myocardial infarctions, and an eosinophil count of 5,000/l represents the first case of severe eosinophilic interstitial nephritis associated with idiopathic hypereosinophilic syndrome, a condition that involves the heart frequently and the kidney rarely. The patient’s eosinophilia and renal failure responded to prednisone (NDT Plus 2:379).
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The DRESS syndrome (drug rash with eosinophilia and systemic symptoms), commonly manifested as hepatitis and pneumonia but rarely affecting the kidney, presented as acute eosinophilic interstitial nephritis and acute tubular necrosis (serum creatinine 9 mg/dl) in a patient treated with sulfasalazine for pneumocystis pneumonia. There was complete recovery after several hemodialyses and treatment with prednisone 80 mg/d (Nephrol Dial Transpl 24:2,940).
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Clarithromycin given for pneumonia also caused AKI (serum creatinine 2.2 mg/dl), eosinophilia, and a patchy eosinophilic interstitial nephritis, but this presented edema, rash, and characteristic features of minimal change disease — edema, serum albumin 1.9 g/L, urinary protein 9 g/d, widespread foot process fusion, and prompt response to prednisolone (NDT Plus:382).