[From mice to men - insights from the hantavirus epidemic in 2010]. / Von Mäusen auf Menschen - Erkenntnisse aus der Hantavirus-Epidemie 2010.

HISTORY AND ADMISSION FINDINGS: With 2017 notified cases the largest hantavirus epidemic in Germany has occurred in 2010. We report on two interesting cases illustrating the wide range of the individual clinical course and the diagnostic problems in hantavirus disease. The first patient was a seriously ill 44-year-old man who needed dialysis after an onset of flu-like symptoms with oliguria. An initially negative result of a hantavirus serology focused attention on rapidly progressive glomerulonephritis. The second patient, a 22-year-old man, presented with severe neurological symptoms with seizures. TREATMENT AND COURSE: Pathological examination of the renal-biopsy specimen in Case 1 reportedly showed the typical pattern of tubulointerstitial damage in the renal cortex and the outer medulla as in hantavirus infection. In a repeated analysis Puumala virus RNA as a marker of acute infection was found. After dialysis and administration of higher-dose systemic glucocorticoids the patient slowly recovered. In Case 2 the severe neurological symptoms caused a complete neurological diagnostic with lumbar puncture and MRI before the detection of specific antibodies and Puumala virus RNA showed that nephropathia epidemica was the disease. The patient recovered after 10 days. CONCLUSION: Because of the variability of symptoms and the extrarenal manifestations of the disease the nephropathia epidemica can occasionally cause problems of differential diagnosis. A rapid diagnosis is important because of the urgent differentiation of other renal diseases with bad prognosis.

[Expert consensus statement on interventional renal sympathetic denervation for hypertension treatment]. / Interventionelle renale Sympathikusdenervation zur Behandlung der therapieresistenten Hypertonie.

This commentary summarizes the expert consensus and recommendations of the working group 'Herz und Niere' of the German Society of Cardiology (DGK), the German Society of Nephrology (DGfN) and the German Hypertension League (DHL) on renal denervation for antihypertensive treatment. Renal denervation is a new, interventional approach to selectively denervate renal afferent and efferent sympathetic fibers. Renal denervation has been demonstrated to reduce office systolic and diastolic blood pressure in patients with resistant hypertension, defined as systolic office blood pressure ≥ 160 mm Hg and ≥ 150 mm Hg in patients with diabetes type 2, which should currently be used as blood pressure thresholds for undergoing the procedure. Exclusion of secondary hypertension causes and optimized antihypertensive drug treatment is mandatory in every patient with resistant hypertension. In order to exclude pseudoresistance, 24-hour blood pressure measurements should be performed. Preserved renal function was an inclusion criterion in the Symplicity studies, therefore, renal denervation should be only considered in patients with a glomerular filtration rate > 45 ml/min. Adequate centre qualification in both, treatment of hypertension and interventional expertise are essential to ensure correct patient selection and procedural safety. Long-term follow-up after renal denervation and participation in the German Renal Denervation (GREAT) Registry are recommended to assess safety and efficacy after renal denervation over time.

Long-term ciclosporine A treatment in adults with minimal change nephrotic syndrome or focal segmental glomerulosclerosis.

To evaluate the efficacy and safety of long-term ciclosporine A (CSA) treatment in idiopathic nephrotic syndrome, we prospectively followed immunosuppressive therapy in 22 nephrotic adults for a median of 32 months (range 7-91 months) and obtained repeat renal biopsies. CSA induced complete remission in 60.0% and 14.3% of patients with minimal change nephrotic syndrome (MCNS) (n = 7), respectively. In addition, partial remissions were achieved in 20.0% of patients with MCNS and in 42.9% of patients with FSGS. Resolution of proteinuria was strictly CSA-dependent and no sustained remission occurred following withdrawal, thereby requiring long-term treatment in 18 patients. In 10 patients CSA was administered for more than 43 months. During maintenance therapy the antiproteinuric effect of CSA was preserved and renal function as well as blood pressure remained stable in patients with MCNS, whereas renal function deteriorated in two patients with FSGS due to progression of the underlying renal disease. Renal biopsies revealed slight signs of CSA toxicity in four patients. However, in no case loss of renal function was attributable to these lesions. In conclusion, the present data suggest that long-term maintenance treatment of MCNS with CSA is efficacious and safe at least for a period of up to 43 months. In contrast, CSA has some effect on proteinuria in FSGS, but the results are less favorable.

Which bicarbonate concentration is adequate to lactate-buffered substitution fluids in maintenance hemofiltration?

We investigated the metabolic and hemodynamic effects of a lactate- and a bicarbonate-buffered (bicarbonate concentration 31.4 mmol/l, type I) hemofiltration substitution fluid in a prospective crossover study of 3 weeks each in 11 patients on maintenance hemofiltration. The lactate-buffered hemofiltration (lactate concentration 34-44.5 mmol/l) lead to hyperlactatemia in all patients without signs of overt lactic acidosis but showed a better control of acid-base balance (pH, base excess, standard bicarbonate) than the type I bicarbonate-buffered fluid (p < 0.01). In 6 patients a higher concentration of bicarbonate- (39.7 mmol/l, type II) buffered fluid was tested. The parameters of acid-base balance showed a better control during type II than during type I bicarbonate hemofiltration and were similar to the lactate-buffered phase. Plasma lactate levels between type I and type II bicarbonate hemofiltration were not different. Also in the steady state phase of the treatment (days 7-9 [week 3]) parameters of acid-base balance rose more to normal values during type II than during lactate-buffered hemofiltration. Hemodynamic parameters showed no differences between the three types of buffers used. Furthermore, also the type II bicarbonate fluid was well tolerated. Bicarbonate in a higher concentration (39.7 mmol/l) proved to be a safe and practical alternative to lactate-buffered hemofiltration.

Serial kidney biopsies in patients with nephrotic syndrome treated with cyclosporin.

A total of 21 patients with severe steroid-resistant or steroid-dependent nephrotic syndrome have been treated with cyclosporin (CsA) over a period of 6 to 71 months. A permanent treatment was started in patients with complete [c] (proteinuria less than 0.3 g/day) or partial [p] (0.3 to less than 3.0 g/day) remission. In four cases proteinuria was markedly reduced but still greater than 3 g/day. Informed consent was obtained and all patients agreed to further control biopsies. Out of 14 patients treated for longer than 6 months, a fall in creatinine clearance was seen in three cases, including two patients with focal sclerosis who required dialysis treatment. Control biopsies were performed once in 11 and twice in seven patients. In two cases definite CsA-related damage was diagnosed after 1 and 24 months of treatment. Possible CsA-induced damage could not be excluded in three additional cases. In all other biopsies no CsA-related alterations could be demonstrated up to 47 months of treatment. The mean values of the creatinine clearance showed no deterioration. The drop off in a few cases has been related to the basic disease.

Long-term treatment of minimal-change nephrotic syndrome with cyclosporin: a control biopsy study.

Seven patients with minimal-change nephrotic syndrome confirmed by renal biopsy were treated with cyclosporin (CsA). Four patients had frequent relapses and three others had primary steroid resistant nephrotic syndrome. Corticosteroids were discontinued as soon as CsA whole blood trough values of 200-500 ng/ml (RIA method) were reached. A full remission, defined as complete disappearance of proteinuria, was achieved in five patients under this treatment. In the two other patients proteinuria was reduced. Two patients experienced an acute episode of dose-dependent nephrotoxicity; however, overall renal function, as determined by the creatinine clearance, was stable. Control biopsies in five patients after a mean treatment period of 10 months showed no significant vascular or interstitial toxicity.

Torasemide for diuretic treatment of advanced chronic renal failure.

In a double-blind randomized clinical trial the efficacy and safety of oral high-dose torasemide (1-isopropyl-3- ([4-(3-methyl-phenylamino)pyridine]-3-sulfonyl)urea, T) therapy was compared with that of furosemide (F) in 10 patients with advanced chronic renal failure. The efficacy on edema, fluid and electrolyte balance including the influence on renin-angiotensin-aldosterone system and cochlear function was evaluated. Patients were randomly allocated to either 500 mg F/d (group 1) or 200 mg T/d (group 2). After 14 days of treatment doses were doubled in each group for further 14 days. With respect to the 2.5 times lower dose of T the clinical effect of both drugs on edema, fluid and sodium excretion was equipotent. Significant differences were noted on calciuresis. Serum calcium levels were reduced with F, while T had no influence on calcium balance. A significant increase in plasma renin activity (PRA) was observed after F, whereas T had no raising effect on PRA. No significant alteration of plasma aldosterone concentration occurred with T or F. No adverse effects were noted in both groups. Serial audiometries showed no significant impairment of cochlear function with both drugs. In conclusion, these results indicate that high-dose T is efficient and safe in the treatment of advanced chronic renal failure. The lack of a calciuric effect with T can be regarded as an advantage in patients with hypocalcemia in chronic renal failure.