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Despite advanced techniques of renal replacement therapy as well as improved medical care and control over the last decade, the overall mortality of patients with "internal" nontraumatic acute renal failure (ARF) requiring replacement therapy is still high. In a retrospective study we compared causes of nontraumatic ARF, risk factors for the development of renal failure and mortality rates in patients with nontraumatic ARF, who received hemodialysis therapy from 1981 to 1990 and from 1991 to 2000. 510 patients with nontraumatic ANV requiring hemodialysis were evaluated, 278 patients in 1981-1990 and 232 patients in 1991-2000. In both groups the chronic risk factors for ANV such as hypertension, diabetes mellitus, chronic cardiac failure, chronic hepatic failure and pre-existing renal impairment and the causes of a traumatic ARF were compared. In addition, concomitant sepsis and multi-organ failure as prognostic parameters as well as mortality rates dependent on the causes of ARF were evaluated. In the latter period, there was a significant reduction in the prevalence of acute glomerulonephritis (3.0 versus 8.3%, p < 0.05) and acute interstitial nephritis (2.6 versus 7.6%, p < 0.05) as well as acute pancreatitis (1.7 versus 7.6%, p < 0.01) as causes of ARF. On the other hand, the prevalence of drug-induced ARF increased during the latter period (10.8 versus 4.7%, p < 0.05). Other etiologies of nontraumatic ARF did not significantly differ between the two decades. Patients treated from 1991 to 2000 had chronic risk factors for the development of ARF, namely diabetes (14.6 versus 6.8%), coronary artery disease (28.0 versus 9.3%) and pre-existing renal impairment (51.7 versus 17.6%, p < 0.001), more frequently than did patients dialysed from 1981-1990. The prevalence of sepsis and multi-organ failure was approximately the same in both periods. The overall mortality (41.8 versus 44.6%, NS) and mortality secondary to causes of nontraumatic ARF were similar in both periods. In summary: the prevalence of several causes of nontraumatic ARF has changed during the last decades. Furthermore, patients treated in the 90's had chronic risk factors for renal failure, namely diabetes and pre-existing renal impairment as well as coronary artery disease, more frequently than did subjects treated in the preceding time period. The prognosis of the patients has not been significantly improved.

History and Admission Findings: A 47-year-old woman with poorly controlled diabetes mellitus (HbA1C 9.2%, fasting blood glucose > 200 mg/dl) had complained of moderately severe stabbing pain in the left abdomen. On admission there were no abnormal findings on abdominal palpation., Investigations: Abdominal ultrasound and computed tomography (CT) revealed a partly solid partly cystic well-circumscribed space-occupying lesion, about 15 cm in diameter, in the left abdomen, extending from the lower third of the kidney into the pelvis., Diagnosis, Treatment and Course: Biopsy of the lesion showed chronic granulating inflammation with foamy histiocytes (Hansemann macrophages) as characteristic substrate of extensive malakoplakia. Despite the size of the lesion it was not excised but long-term treatment with ciprofloxacin undertaken. At the same time, the diabetes was carefully controlled with ordinary insulin. Ten months later there was no longer any evidence of the lesion by ultrasound and CT., Conclusions: Even extensive malakoplakia can be successfully treated with ciprofloxacin. Poorly controlled diabetes together with a weak immune status (CD4/CD8 < or = 1) may have favoured the occurrence of malakoplakia.

Atraumatic rhabdomyolysis with consecutive oliguric renal failure occurred in a 67-year-old man with chronic renal insufficiency in the pre-dialysis phase after four years of therapy with lovastatin without complications. Diuresis remained low after normalization of the muscle enzymes, and the patient required chronic hemodialysis. This case report shows that lovastatin-associated rhabdomyolysis with consecutive myoglobinuric renal failure can be seen also after long-standing lovastatin therapy. In pre-existing renal insufficiency this can lead to earlier requirement of chronic dialysis treatment.

In 50 type-1 and 50 type-2 diabetic patients serum uric acid levels were measured. Type-1 diabetics showed significantly lower serum uric acid levels in comparison to type-2 diabetics (p < 0.02). This significant difference has been observed in both women (p < 0.001) and men (p < 0.01). Serum uric acid level was lower in type-1 diabetics than in healthy controls but only in diabetic men the difference was statistically significant (p < 0.001). Male type-2 diabetic patients showed serum uric acid levels similar to the controls, but levels were higher in women with type-2 diabetes (p < 0.001). The results of this study show that in type-1 diabetic patients the serum uric acid levels are lower in normal (creatinine clearance > or = 80 ml/min) as well as in slightly decreased (creatinine clearance < 80 ml/min) glomerular filtration rate. But in type-2 diabetic patients the serum uric acid levels were significantly higher when glomerular filtration rate was below 80 ml/min in contrast to normal renal function (p < 0.05).

Over a six-week period a 60-year-old patient had several unexplained intoxication-like episodes. He finally had severe abdominal cramps with changes in the level of consciousness and oligoanuric renal failure (creatinine 4.7 mg/dl). The history, marked metabolic acidosis (pH 7.15, HCO3- 2.2 mmol/l, pCO2 6.6 mmHg) as well as raised anion residue (43 mmol/l) and the presence of oxalates in urine suggested poisoning by ethylene glycol contained in antifreeze liquid. Intensive haemodialysis adequately eliminated ethylene glycol and its toxic metabolites (glycol aldehyde, glycolic acid). Renal function returned within 10 days, although the concentrating power of the kidney remained impaired for several weeks because of interstitial nephritis. The intoxication had been caused by a defective heating-pipe system from which the antifreeze had leaked into the hot-water boiler (the patient had habitually prepared hot drinks by using water from the hot-water tap). Gas chromatography demonstrated an ethylene glycol concentration of 21 g per litre of water.

In patients with essential hypertension increased albumin excretion in the urine compared to healthy controls is well known. In 38 patients (age: Mean +/- SD = 37 +/- 16 yr, f: m = 19:19) with benign essential hypertension and normal renal function (creatinine clearance: Mean +/- SD = 99 +/- 16 ml/min) we found a mean urinary albumin excretion of 79 +/- 61 mg/24 h in comparison to 14 +/- 13 mg/24 h (p less than 0.01) in 10 healthy controls (age: Mean +/- SD = 35 +/- 14 yr, f: m = 5:5). In 13 patients with hypertension urinary albumin excretion was increased (greater than 25 mg/24 h) in a subclinical range (microalbuminuria), the other 25 hypertensive patients had normoalbuminuria. Comparing the hypertensive patients with and without microalbuminuria, those with elevated albumin excretion were older (age: Mean +/- SD = 42 +/- 12 yr vs. 32 +/- 19 yr), had a longer average duration of hypertension (8 +/- 5 yr vs. 5 +/- 4 yr) and a higher prevalence both of hypertensive retinopathy (77% vs. 28%) and of abnormalities in the electrocardiogram (23% vs. 4%) than those with normal albumin excretion. The difference in the prevalence of hypertensive retinopathy (grade I and II) was statistically significant (p less than 0.05). Furthermore the patients with microalbuminuria required a more intensive antihypertensive therapy than those with normoalbuminuria, 46% requiring triple drug therapy as opposed to 24% in the latter group. Thus the demonstration of microalbuminuria in patients with benign essential hypertension is associated with a higher prevalence of funduscopic and electrocardiographic abnormalities, and therefore can be considered as an indicator of early vascular damage in essential hypertension.

In a retrospective study the frequency of hypokalemia was investigated in a large group of hospitalized patients. In a period of 1 year 33,426 patients were hospitalized, of these 1,177 (3.52%) revealed serum potassium level of less than or equal to 3.0 mmol/l. On admission to the hospital 592 (50.3%) showed serum potassium levels within normal range and developed their hypokalemia in the hospital. A severe hypokalemia equal or lower 2.5 mmol/l was observed only in 0.54% of the patients. Hypokalemia was frequently associated with cardiovascular, gastrointestinal and urogenital diseases following by diabetes mellitus and polytraumas. The main causes of hypokalemia were diuretics and gastrointestinal potassium loss. Severe hypokalemia (less than or equal to 2.5 mmol/l) is a predisposing factor for the occurrence of ectopic ventricular activity in patients with preexisting myocardial lesions like left ventricular hypertrophy or after myocardial infarction. Therefore in patients with preexisting myocardial lesions and severe hypokalemia potassium replacement therapy may be needed.