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Case Report: A 69-year-old man was admitted to the authors' hospital with an increase of plasma creatinine from 1.4 up to 4.9 mg/dl within 4 months and the clinical complaints of painful purple toes, recurrent epistaxis and disturbances of equilibrium. His past medical history was remarkable for three transient ischemic attacks and the diagnosis of a metabolic syndrome. Magnetic resonance imaging showed vasculitis-like lesions in the brain. Eosinophilia and tubular proteinuria were detected. Renal insufficiency was caused by cholesterol crystal embolism, as shown both by skin and renal biopsy. Aortic plaques were identified as the putative source of cholesterol embolization., Conclusion: In case of rapidly progressive renal failure, cholesterol crystal embolism must be considered even without preceding angiography.

Cidofovir is an antiviral drug with activity against a wide array of DNA viruses including poxvirus. The therapeutic use of cidofovir is marred by a dose-limiting side effect, nephrotoxicity, leading to proximal tubular cell injury and acute renal failure. Treatment with cidofovir requires the routine use of prophylactic measures. A correct knowledge of the cellular and molecular mechanisms of cidofovir toxicity may lead to the development of alternative prophylactic strategies. We recently cared for a patient with irreversible acute renal failure due to cidofovir. Renal biopsy showed tubular cell apoptosis. Cidofovir induced apoptosis in primary cultures of human proximal tubular cells in a temporal (peak apoptosis at 7 days) and concentration (10-40 microg/ml) pattern consistent with that of clinical toxicity. Apoptosis was identified by the presence of hypodiploid cells, by the exposure of annexin V binding sites and by morphological features and was associated with the appearance of active caspase-3 fragments. Cell death was specific as it was also present in a human proximal tubular epithelial cell line (HK-2), but not in a human kidney fibroblast cell line, and was prevented by probenecid. An inhibitor of caspase-3 (DEVD) prevented cidofovir apoptosis. The survival factors present in serum, insulin-like growth factor-1 and hepatocyte growth factor, were also protective. The present data suggest that apoptosis induction is a mechanism contributing to cidofovir nephrotoxicity. The prophylactic administration of factors with survival activity for tubular epithelium should be further explored in cidofovir renal injury.

When confronted by the combination of initial high fever associated with intense malaise, splenomegaly, elevated levels of transaminases, and acute renal failure, consideration must be given to the differential diagnosis of leptospirosis even in Germany. As a rule, the diagnosis is confirmed by serological testing based on the titer curve. Renal involvement is frequent, but usually has a good prognosis, especially if jaundice has not developed. Treatment with doxycycline or penicillin can shorten the disease course and exudation, possibly also the nephritis, or hinder it.

Case Report: An 83-year-old patient was admitted to our hospital because of gastrointestinal symptoms, mental confusion and dysarthria. The patient suffered from type 2 diabetes mellitus and was taking metformin. A mild renal insufficiency was known. On admission, we found impaired consciousness, Kussmaul breathing, a body temperature of 32.1 degrees C, and hemodynamic instability. Laboratory testing revealed lactic acidosis (pH 6.71, base excess--30, standard bicarbonate 4.0 mmol/l, lactate 24.4 mmol/l) and acute renal failure with a creatinine of 10.6 mg/dl and blood urea nitrogen of 134 mg/dl. Electrolytes were not altered; the blood glucose was elevated (147 mg/dl). According to history, physical examination, and laboratory testing the diagnosis metformin-induced lactic acidosis with acute renal failure was made. This diagnosis was confirmed by an elevated level of metformin. As soon as possible a bicarbonate hemodialysis was initiated. After 8 hours of hemodialysis the acid-base metabolism was almost balanced and the vigilance of the patient normalized. No further sessions of hemodialysis were needed and insulin therapy was started., Conclusions: Metformin-induced lactic acidosis is a common side effect in patients with renal insufficiency. For an early diagnosis, clinical symptoms of intoxication should be well known by physicians and patients. First-line therapy for correction of lactic acidosis and effective elimination of metformin is bicarbonate hemodialysis. Sodium bicarbonate infusions are not able to correct the acid-base metabolism sufficiently. For prevention the renal function should be monitored closely and metaformin therapy should be stopped, if a deterioration of renal function is observed.