Acute tubular proteinuria

A 57-year-old man with a history of alcohol abuse developed acute respiratory failure and was given lorazepam up to 18 mg/hour during alcohol withdrawal (17). On day 43 (cumulative intravenous lorazepam dose 4089 mg, containing about 220 ml of polyethylene glycol 400), he developed oliguric acute tubular necrosis with proteinuria and granular casts. 

Medications in this class include delavirdine, efa-virenz, and nevirapine. Similar to the NRTls, these agents bind to viral reverse transcriptase and block DNA polymerase activity. A key difference is that NNRTIs do not require intracellular phosphorylation and are not incorporated into viral DNA. Clinically significant kidney toxicities or specific fluid-electrolyte complications have not been reported with this class of agents. In the rat model, efavirenz was associated wifh a species specific dependent kidney toxicity which occurred secondary to the development of a unique glutathione conjugate produced as a metabolite of efavirenz associated with renal tubular epifhelial cell necrosis [125-126]. This toxicity has not been observed in humans. One patient was recently reported to have reversible nephrotic-range proteinuria attributed to efavirenz use, in which a kidney biopsy showed diffuse podocyte foot process effacement [127]. Another report noted the development of rhabdomyolysis and acute tubular necrosis as a result of a drug interaction between delavirdine and atorvastatin [128]. Kidney toxicity due to nevirapine has not been reported. 

Patients with nephrogenic diabetes insipidus often have polydipsia and polyuria (see Chap. 49). They adapt well to their urinary-concentrating defect and these concerns are usually minimal. Acute tubular necrosis is frequent in the setting of acute hthium toxicity. Urinalysis may show moderate proteinuria, a few red and white blood cells, and granular casts. Renal function usuahy returns to baseline values after hthium concentrations are reduced to the therapeutic range. Nephrotoxicity may develop insidiously and be recognized by rising BUN or creatinine concentrations or the onset of hypertension. The urinalysis may show mild proteinuria and a few red and white blood cells. 

Nephrotoxicity (6% to 7% incidence) includes proteinuria, hypokalemia, acidosis, and acute tubular necrosis—usually reversible, but enhanced by vancomycin, amphotericin B, cisplatin, and cyclosporine. 

Since intratubular hydrostatic pressure does not differ significantly from controls in euvolemic and volume expanded animals, it is unlikely that intratubular obstruction plays an important role in early, cispl-atin-induced acute renal failure. Following withdrawal of the drug, renal insufficiency stabilizes but remains indefinitely impaired. The cisplatin-induced hypofil-tration is usually associated with tubular proteinuria. Severe salt-wasting with orthostatic hypotension has been observed after cisplatin administration in a minority of patients [18]. 

Proteinuria, hematuria, and acute tubular necrosis have been reported in severely intoxicated patients. Gouty nephropathy may occur in chronically treated patients. Azoospermia has been reported with chronic use. 

A. Nephrotoxicity (eg, acute tubular necrosis, proteinuria, and hematuria) may be minimized by adequate hydration, estabiishment of adequate urine flow, avoidance of excessive doses, and iimitation of continuous administration to 5 or fewer days. Laboratory assessment of renai function should be performed daily during treatment for severe intoxication and after the second and fifth days in other cases. 

Kidney hsdogenated hydrocaibcarbon tetrachloride), toluene, dioxane, diethylene glycol, ethylene glycol, glycol ethers, conjugates of trichloroethylene acute tubular necrosis, glomerular and tubular dysfunctions (e.g., albuminuria, proteinuria), glomerulonephritis, note modification of solvent effects caused by renal dysfunctions possible... 

Renal Effects. Acute nephritis with albuminuria and oliguria, polyuria, and nitrogen retention were observed in individuals after application of a salve that contained potassium chromate. These effects disappeared in individuals who survived. Autopsy of people who died revealed hyperemia and tubular necrosis (Brieger 1920). Acute nephritis with polyuria and proteinuria were also described in a man who was admitted to a hospital with skin ulcers on both hands due to dermal exposure to ammonium dichromate in a planographic printing establishment where he had worked for a few months (Smith 1931). A 49-year-old man with an inoperable carcinoma of the face was treated with chromic acid crystals. Severe nephritis occurred after treatment with the chromium(VI) compound. Urinalysis revealed marked protein in the urine. Death resulted 4 weeks after exposure. A postmortem examination of the kidneys revealed extensive destruction of the tubular epithelium (Major 1922). 

AIN is characterized by fever, eosinophilia, hematuria, mild proteinuria and skin rash occur an average of 15 days after exposure (range 2-40). Rising serum creatinine concentration and acute renal failure with oliguria develop in about 50% of AIN cases, especially in older patients. Histologically, interstitial granulomas and variable degrees of tubular necrosis may be seen on renal biopsy. 

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