Henoch-Schönlein purpura in adults is not uncommon in elderly patients with an adverse prognosis.

BACKGROUND: Henoch-Schönlein purpura (HSP) is a fairly common disease in children and adolescents. There are only limited data available for adults. METHODS: A retrospective analysis was conducted to study renal manifestations in patients with HSP treated in our institution between 1982 and 2007. We divided our adult cohort according to age - under or over 60 years - to examine differences in elderly patients. RESULTS: HSP was identified in 2.2% of patients referred to us for kidney biopsy. Purpuric lesions and renal involvement were found in all patients. An important triggering factor for the development of HSP in our series was chronic alcohol intake. Forty percent of our patients fulfilled the WHO criteria for alcoholics. Renal involvement was particularly prominent in patients over 60 years of age. At disease onset, estimated glomerular filtration rate (eGFR) was 63% lower in the elderly. Within a median follow-up of 8 years, renal function was significantly better in younger adults than in the elderly. 32% of the elderly have shown Modification of Diet in Renal Disease (MDRD) < 20 ml/min/1.73 m2 in contrast to only 7% in patients < 60 years. Furthermore, significantly more elderly patients reached end-stage renal failure. CONCLUSION: The data indicate that renal manifestation of HSP in the elderly is severe and its outcome relatively poor, and worsens when compared to patients < 60 years.

Optimal blood pressure control versus additional immunosuppressive therapy in idiopathic membranous nephropathy - a retrospective analysis.

The treatment of idiopathic membranous nephropathy (MN) with nephrotic syndrome comprises immunosuppressive therapy and antihypertensive treatment with the blockade of the renin-angiotensin system (RAS). Given the relatively benign natural history of MN, an immunosuppressive-free therapeutic regimen should be considered as the primary treatment option. In a single-center, retrospective analysis we compared the outcome of 54 patients with biopsy-proven idiopathic MN 12, 24 and 60 months after initiation of therapy. All patients had RAS-blocking agents and 36 patients received additionally an immunosuppressive regimen. In both groups the patients initially had a nephrotic proteinuria (median 8.7 vs. 6.0 g/day, n.s.). Median blood pressure reduction was comparable after 12, 24 and 60 months in both groups. The median evolution of proteinuria during therapy after 12, 24 and 60 months was 3.4, 1.7 and 1.1 g/day in the group with immunosuppression compared to 3.0, 1.1 and 0.32 g/day in the non-immunosuppressive group. After 60 months no patient developed endstage renal failure. The number of severe side effects was significantly higher in patients with immunosuppression. Regarding renal function and reduction of proteinuria, patients with idiopathic MN treated without immunosuppressive therapy but with measures to ensure optimal blood pressure control and the full blockade of RAS had a similar outcome after 60 months as compared to patients who received additional immunosuppressive therapy.

[Renal replacement therapy in the intensive care unit]. / Nierenersatztherapie auf der Intensivstation.

Acute renal failure in critically ill patients in the intensive care unit is associated with high morbidity and mortality which is independent of the underlying etiology. Despite improvements in intensive care medicine and renal replacement therapy, patients with acute renal failure have much higher morbidity and mortality rates than patients without acute renal failure in the intensive care unit. In this overview, we summarize the literature on the incidence and mortality of patients with acute renal failure in the intensive care unit. Furthermore, we discuss timing of the initiation of renal replacement therapy, patient outcome with different renal replacement therapies and the adequate dialysis dose to be delivered.

Real-time contrast-enhanced sonography of renal transplant recipients predicts chronic allograft nephropathy.

Real-time contrast-enhanced sonography (RT-CES) can assess microvascular tissue perfusion using gas-filled microbubbles. The study was performed to evaluate the feasibility of RT-CES in detecting chronic allograft nephropathy (CAN) in comparison to color Doppler ultrasonography (CDUS). A total of 26 consecutive renal transplant recipients were prospectively studied using RT-CES and conventional CDUS. Transplant tissue perfusion imaging was performed by low-power imaging during i.v. administration of the sonocontrast Optison. Renal tissue perfusion was assessed quantitatively using flash replenishment kinetics of microbubbles to estimate renal blood flow A *beta (A = peak signal intensity, beta= slope of signal intensity rise). In contrast to conventional CDUS resistance and pulsatility indices, renal blood flow estimated by CES was highly significant related to S-creatinine (r =-0.62, p = 0.0004). Determination of renal blood flow by CES reached a higher sensitivity (91% vs. 82%, p < 0.05), specificity (82% vs. 64%, p < 0.05) and accuracy (85% vs. 73%, p < 0.05) for the diagnosis of CAN as compared to conventional CDUS resistance indices. Perfusion parameters derived from RT-CES significantly improve the early detection of CAN compared to conventional CDUS. RT-CES using low-power real-time perfusion imaging is a feasible method to evaluate microvascular perfusion in renal allograft recipients.

Severe rhabdomyolysis and renal failure triggered by a sauna visit in sickle cell trait: a case report.

Sickle cell trait (SCT) is an usually asymptomatic hemoglobinopathy. Cases of sudden excertional deaths in individuals with SCT have been described. We here report an exceptional case of excessive rhabdomyolysis and acute renal failure triggered by a sauna visit in a 29 year-old African American with SCT.

Blood pressure profile and treatment quality in liver allograft recipients-benefit of tacrolimus versus cyclosporine.

Organ transplant recipients display a high cardiovascular mortality rate. The type of immunosuppression has a major impact on cardiovascular risk factors (e.g., hypertension [HTN]). We assessed 24-hour blood pressure (BP) and metabolic profiles in a cohort of 106 long-term liver allograft recipients treated with either tacrolimus (Tac) or cyclosporine (CyA). The median age of patients was 50.8 years (range, 11 to 77) and the median time of follow-up was 65.4 months (ranges 12 to 168). Immunosuppression included low-dose steroids and either Tac (n = 46) or CyA (n = 60). Twenty-four-hour BP measurements revealed a significant difference in systolic BP (127.1 mmHg [94 to 163] Tac versus 132.7 mmHg [103 to 177] CyA; P <.03), and in mean arterial and diastolic blood pressures. In addition, the relative number of normotensive patients was significantly higher among Tac-treated patients (69.6% versus 34.8%). It is of note that the true incidence of HTN was higher after the number of patients with a pathological 24-h BP measurement was added to the initial number of patients already known to have HTN. No less than 76.4% of all long-term liver transplanted patients showed HTN. The results were unrelated to cumulative steroid dosage, frequency of antirejection therapy or underlying primary liver disease. In summary, immunosuppression-induced HTN is more common in CyA-treated than Tac-based regimens. Moreover, we found a substantial lack of detection of HTN in long-term liver transplant patients who received an insufficient quality of antihypertensive treatment. These findings have implications for the early diagnosis and treatment of HTN in liver transplant recipients.

Hypertension after renal transplantation.

With current immunosuppression elevated blood pressure is found in almost 90% of renal graft recipients. Major causes of this finding are impairment of renal function, secondary to chronic allograft nephropathy or (less frequently) recurrence of primary renal disease, the use of calcineurin inhibitors as immunosuppresants, uncontrolled renin secretion by the shrunken kidneys of the recipient, stenos- ing lesions of the transplant artery (or the upstream arteries of the recipient), polycytemia and (genetic predisposition to) hypertension of the graft donor. Even minor degrees of blood pressure elevation have a significant impact on survival of the recipient and on graft survival, presumably by amplifying vascular injury to the graft. In this respect, elevation of systolic blood pressure and an abnormal circadian blood pressure profile are of particular relevance. In contrast to previous opinion, ACE inhibitors are indicated in the treatment, but, given the causal role of sodium retention in graft vasoconstriction, diuretics and calcium channel blockers remain main stays of antihypertensive treatment in the renal allograft recipient.

[Acute renal failure and hypertension crisis after a technoparty]. / Akutes Nierenversagen und Hochdruckkrise nach Technoparty.

HISTORY: A 22 year old patient had noted progressive flank pain without recognizable urinary abnormalities for five days. INVESTIGATIONS: A urologist had noted increased serum creatine (2.1 mg/dl), hypertension (180/100 mmHg) and microhematuria. A post-renal cause was excluded by excretory urography. An interview revealed that the patient had consumed cocaine on weekends since age 19; the acute episode was preceded by a rave party with consumption of a total of 3 g of street quality cocaine. DIAGNOSIS AND TREATMENT: Because of microhematuria with a suggestive nephritic urinary sediment, the patient underwent renal biopsy. It showed acute tubular necrosis and interstitial edema, but no signs of glomerulonephritis and negative immunohistology. The patient received antihypertensive treatment. This led to rapid reversal of elevated serum creatinine and microhematuria was noted, but hypertension persisted. Currently the patient receives ACE inhibitors. CONCLUSION: Similar to what is seen in the US, cocaine use has to be considered in the differential diagnosis of acute renal failure with hypertension.

[Microalbuminuria is an early marker for increased morbidity and mortality]. / Mikroalbuminurie als früher Marker für eine erhöhte Morbidität und Mortalität.

Recent studies have shown the beneficial effects of a blockade of the renin-angiotensin system (RAS) not only for blood pressure reduction but also end organ protection. One of the markers that is closely correlated with the increased cardiovascular risk is microalbuminuria. A common mediator for the development of both, microalbuminuria and end organ damage seems to be Angiotensin II, the blockade of which apparently reduces microalbuminuria as well as end organ damage. Therefore we had a closer look into pathophysiology of microalbuminuria and the relevance for end organ damage and discuss current medical strategies to alleviate these diseases.

[Diabetes, hypertension and microalbuminuria in primary care]. / Diabetes, Hypertonus und Mikroalbuminurie in der allgemeinärztlichen Versorgung.

Microalbuminuria has been widely appreciated in recent years to be a valuable risk marker for an increased cardiovascular disease morbidity and mortality. Thus guidelines for the treatment of type-2-diabetes in Germany and the US recommend an annual screening as soon as the diagnosis of diabetes is established and a quarterly control when microalbuminuria is present. While nationally representative epidemiologic data from the US have been available, data from Germany, especially from the primary care sector are missing. This is especially important in light of the gatekeeper function of the primary care physician. The "Hypertension and Diabetes Risk Screening Study" (HYDRA) has been identifying 37.8% of patients with hypertension and diabetes to have a positive dipstick test for microalbuminuria on the study day while only 12.5% of these are diagnosed by the doctor as having nephropathy. These patients additionally show a high burden of associated comorbidities and thus call for early detection and intervention especially because effective therapy is available. Although screening for microalbuminuria is recommended in the guidelines the value of a routine screening for microalbuminuria in primary care is under recognized.

[Nephropathy: an overview for daily practice]. / Nephropathie--ein Uberblick über die tägliche Praxis.

The examination of renal function in the daily practice may give important information on the risk status of a given patient. For example, the diagnosis of microalbuminuria carries high predictive value for a future cardiovascular risk of patients with hypertension, diabetes, congestive heart failure, as well as myocardial infarction. The findings of the Hypertension and Diabetes Screening and Awareness Study (HYDRA) indicate that screening for microalbuminuria is performed not often enough in patients with diabetes or hypertension, respectively, and a positive screening finding often does not trigger necessary consequences as for additional diagnosis or therapy.

Blood pressure after renal transplantation.

Hypertension is extremely common in renal allograft recipients, mainly as the result of impaired renal function and cyclosporin A therapy. Blood pressure is a powerful independent predictor of longterm graft outcome. This adverse effect is presumably mediated by both hemodynamic and non-hemodynamic factors. There is also evidence for activation of the renin angiotensin system in the renal allograft. Antihypertensive treatment is of known benefit on graft outcome in experimental models, but this has so far not been documented in clinical trials. Proteinuria is another independent predictor of longterm graft outcome. There is recent documentation of a specific antiproteinuric effect of ACE inhibitors on proteinuria which is of interest since proteinuria is an independent predictor of longterm graft outcome.

Effects of acute ACE inhibition on pulsatile renin and aldosterone secretion and their synchrony.

Pulsatile (burstlike) secretion of renin and aldosterone is positively coupled with a short time lag of about 10 to 20 minutes. We investigated how acute interruption of the renin-angiotensin-aldosterone axis, ie, acute angiotensin-converting enzyme (ACE) inhibition, alters the pattern of renin and aldosterone secretion. Eight healthy men (mean age, 22+/-1 years) were studied while on standardized salt intake. They were allocated on 2 occasions in random order to injection of placebo or 1.25 mg of the ACE inhibitor enalaprilat. Blood samples were obtained every 10 minutes for 24 hours for measurement of plasma renin and aldosterone concentrations. The hormone concentration profiles were analyzed using a multiparameter deconvolution technique; basal (tonic) and pulsatile hormone secretion was assessed. The regularity of pulsatile hormone secretion was analyzed using approximate entropy (ApEn). Cross-correlation and cross-ApEn analysis of renin and aldosterone secretion were performed to assess synchrony. Acute ACE inhibition caused an immediate burst of renin release and, in addition, significantly (P<0.01) increased 24-hour pulsatile and total renin secretion. It did not affect basal (nonpulsatile) renin secretion. The amplitude of renin bursts and the mass of hormone secreted per burst were significantly (P<0.01) increased, whereas the burst frequency (ie, number of secretory events) was unchanged. ApEn analysis revealed significantly (P<0.05) more regular renin secretion after ACE inhibition. In contrast, neither basal nor pulsatile aldosterone secretion was affected by administration of enalaprilat. Cross-ApEn analysis documented not only a maintained pattern of reproducibility (ie, synchrony) but also greater conditional regularity between pulsatile renin and aldosterone secretions with acute ACE inhibition. However, the quantitative strength of hormone coupling (assessed by cross-correlation analysis) was markedly diminished by enalaprilat treatment. The present findings suggest that the renin-angiotensin-aldosterone axis may not be completely uncoupled by acute ACE inhibition or that pulsatile renin and aldosterone secretion is driven by a common signal generator that is unaffected by ACE inhibition. In addition, a background basal and pulsatile aldosterone secretion not regulated by the renin-angiotensin axis may exist.