Copeptin and insulin resistance: effect modification by age and 11 ß-HSD2 activity in a population-based study.

PURPOSE: Arginine vasopressin (AVP) may be involved in metabolic syndrome (MetS) by altering liver glycogenolysis, insulin and glucagon secretion, and pituitary ACTH release. Moreover, AVP stimulates the expression of 11ß-hydroxysteroid-dehydrogenase-type 2 (11ß-HSD2) in mineralocorticosteroid cells. We explored whether apparent 11ß-HSD2 activity, estimated using urinary cortisol-to-cortisone ratio, modulates the association between plasma copeptin, as AVP surrogate, and insulin resistance/MetS in the general adult population. METHODS: This was a multicentric, family-based, cross-sectional sample of 1089 subjects, aged 18-90 years, 47% men, 13.4% MetS, in Switzerland. Mixed multivariable linear and logistic regression models were built to investigate the association of insulin resistance (HOMA-IR)/fasting glucose and MetS/Type 2 Diabetes with copeptin, while considering potential confounders or effect modifiers into account. Stratified results by age and 11ß-HSD2 activity were presented as appropriate. RESULTS: Plasma copeptin was higher in men [median 5.2, IQR (3.7-7.8) pmol/L] than in women [median 3.0, IQR (2.2-4.3) pmol/L], P < 0.0001. HOMA-IR was positively associated with copeptin after full adjustment if 11ß-HSD2 activity was high [ß (95% CI) = 0.32 (0.17-0.46), P < 0.001] or if age was high [ß (95% CI) = 0.34 (0.20-0.48), P < 0.001], but not if either 11ß-HSD2 activity or age was low. There was a positive association of type 2 diabetes with copeptin [OR (95% CI) = 2.07 (1.10-3.89), P = 0.024), but not for MetS (OR (95% CI) = 1.12 (0.74-1.69), P = 0.605), after full adjustment. CONCLUSIONS: Our data suggest that age and apparent 11ß-HSD2 activity modulate the association of copeptin with insulin resistance at the population level but not MeTS or diabetes. Further research is needed to corroborate these results and to understand the mechanisms underlying these findings.

Biomarkers of Tolerance in Kidney Transplantation: Are We Predicting Tolerance or Response to Immunosuppressive Treatment?

We and others have previously described signatures of tolerance in kidney transplantation showing the differential expression of B cell-related genes and the relative expansions of B cell subsets. However, in all of these studies, the index group-namely, the tolerant recipients-were not receiving immunosuppression (IS) treatment, unlike the rest of the comparator groups. We aimed to assess the confounding effect of these regimens and develop a novel IS-independent signature of tolerance. Analyzing gene expression in three independent kidney transplant patient cohorts (232 recipients and 14 tolerant patients), we have established that the expression of the previously reported signature was biased by IS regimens, which also influenced transitional B cells. We have defined and validated a new gene expression signature that is independent of drug effects and also differentiates tolerant patients from healthy controls (cross-validated area under the receiver operating characteristic curve [AUC] = 0.81). In a prospective cohort, we have demonstrated that the new signature remained stable before and after steroid withdrawal. In addition, we report on a validated and highly accurate gene expression signature that can be reliably used to identify patients suitable for IS reduction (approximately 12% of stable patients), irrespective of the IS drugs they are receiving. Only a similar approach will make the conduct of pilot clinical trials for IS minimization safe and hence allow critical improvements in kidney posttransplant management.

EFSUMB Guidelines on Interventional Ultrasound (INVUS), Part II. Diagnostic Ultrasound-Guided Interventional Procedures (Short Version).

This is the second part of the series on interventional ultrasound guidelines of the Federation of Societies for Ultrasound in Medicine and Biology (EFSUMB). It deals with the diagnostic interventional procedure. General points are discussed which are pertinent to all patients, followed by organ-specific imaging that will allow the correct pathway and planning for the interventional procedure. This will allow for the appropriate imaging workup for each individual interventional procedure (Long version/ short version; the long version is published online).

EFSUMB Guidelines on Interventional Ultrasound (INVUS), Part II. Diagnostic Ultrasound-Guided Interventional Procedures (Long Version).

This is the second part of the series on interventional ultrasound guidelines of the Federation of Societies for Ultrasound in Medicine and Biology (EFSUMB). It deals with the diagnostic interventional procedure. General points are discussed which are pertinent to all patients, followed by organ-specific imaging that will allow the correct pathway and planning for the interventional procedure. This will allow for the appropriate imaging workup for each individual interventional procedure (Long version).

Impact of proton pump inhibitor use on magnesium homoeostasis: a cross-sectional study in a tertiary emergency department.

BACKGROUND: To date, the use of proton pump inhibitors (PPIs) has been associated with a low risk of hypomagnesaemia and associated adverse outcomes. We hypothesised that a better risk estimate could be derived from a large cohort of outpatients admitted to a tertiary emergency department (ED). METHODS: A cross-sectional study was performed in 5118 patients who had measurements of serum magnesium taken on admission to a large tertiary care ED between January 2009 and December 2010. Hypomagnesaemia was defined as a serum magnesium concentration < 0.75 mmol/l. Demographical data, serum electrolyte values, data on medication, comorbidities and outcome with regard to length of hospital stay and mortality were analysed. RESULTS: Serum magnesium was normally distributed where upon 1246 patients (24%) were hypomagnesaemic. These patients had a higher prevalence of out-of-hospital PPI use and diuretic use when compared with patients with magnesium levels > 0.75 mmol/l (both p < 0.0001). In multivariable regression analyses adjusted for PPIs, diuretics, renal function and the Charlson comorbidity index score, the association between use of PPIs and risk for hypomagnesaemia remained significant (OR = 2.1; 95% CI: 1.54-2.85). While mortality was not directly related to low magnesium levels (p = 0.67), the length of hospitalisation was prolonged in these patients even after adjustment for underlying comorbid conditions (p < 0.0001). CONCLUSION: Use of PPIs predisposes patients to hypomagnesaemia and such to prolonged hospitalisation irrespective of the underlying morbidity, posing a critical concern.

Determinants of haemodialysis access survival.

BACKGROUND: Vascular access patency is of vital importance for patients requiring haemodialysis. This analysis validates potential risk factors and benefits in patients undergoing vascular access procedures. PATIENTS AND METHODS: Vascular access procedures performed over a two-year period were retrospectively analysed. Clinical data and concomitant medication were retrieved from files as were surgical data following a standardized data capture sheet. Outcome parameters were primary (PP) and secondary patency (SP) as well as freedom from repeated revascularization. Minimal follow-up with functioning access was 679 days. RESULTS: During the observation period, 244 patients (mean age 62.2 +/- 0.9 years, 60.7 % male patients, 36.1 % pre-emptive, 31.1 % late referral) underwent vascular accesses procedures. PP and SP were 35.6 % and 45.6 %, respectively, at 540 days. Presence of diabetes mellitus was associated with decreased PP (OR: 0.6, 95 %-CI: 0.3 - 1.0) and SP (OR: 0.4, 95 %-CI: 0.2 - 0.7), whereas female gender was associated with lower SP (OR: 0.6, 95 %-CI: 0.3 - 0.9) and freedom from repeated revascularization rates (OR: 0.6, 95 %-CI: 0.3 - 1.0). In contrast, presence of hyperparathyreoidism was associated with higher SP (OR: 1.7, 95 %-CI: 1.0 - 3.0) and freedom from repeated revascularization (OR: 1.7, 95 %-CI: 1.0 - 3.0) rates. CONCLUSIONS: Haemodialysis access performs worst in patients with diabetes mellitus and in women. The benefit of hyperparathyroidism should be interpreted as hypothesis generating.

Apparent systemic 11ß-dehydroxysteroid dehydrogenase 2 activity is increased in preeclampsia but not in intrauterine growth restriction.

OBJECTIVE: The enzyme 11ß-dehydroxysteroid dehydrogenase 2 (11ß-HSD2) converts active cortisol (F) to inactive cortisone (E). A reduced 11ß-HSD2 activity in the placenta has been demonstrated for prematurity, low birth weight, and preeclampsia. We hypothesized that disturbed placental function rather than a maternal response contributes to decreased 11ßHSD2 activity as reflected by a diminished conversion of F to E. Hence, the aim of the present study was to estimate the systemic activity of 11ß-HSD2 throughout gestation and in pregnancies complicated by preeclampsia (PE) and intrauterine growth restriction (IUGR) by calculating maternal serum F/E ratios. METHODS: A total of 188 maternal serum samples were analyzed for nine glucocorticoid metabolites by gas chromatography-mass spectrometry (GC-MS) and F/E ratios were calculated. Study Group A: In a longitudinal set 33 healthy pregnant women were analyzed at three different time points throughout gestation and one postpartum. Study Group B: Cross-sectionally additional 56 patients were enrolled. We compared patients with PE (N = 14) and IUGR (N = 14) with gestational age matched healthy controls (CTRL = 28). RESULTS: Group A: The apparent 11ß-HSD2 activity dropped in the second trimester being restored to first trimester levels (P value = 0.016). Group B: The 11ß-HSD2 activity was high in PE (P value < 0.05) but not in the IUGR group as compared to CTRL. CONCLUSION: The increased apparent serum 11ß-HSD2 activity observed with advancing gestation in normal pregnancy may reflect an elevated general increase in enzyme activity due to a higher placental mass. The high systemic 11ß-HSD2 activity in PE but not in IUGR however suggests an increased F deactivation in maternal tissue in PE rather than in the placenta since placental insufficiency in the absence of PE does not significantly alter F/E ratio.

[Calcium and blood pressure]. / Kalzium und Blutdruck.

The regulation of blood pressure is complex with several organs being involved. Intracellular calcium plays a crucial role in the regulation of cardiovascular functions: An increased influx of calcium into the vascular smooth muscle cells leads to an augmental muscular tone and therefore to an increased vascular resistance and rise in blood pressure. Parathormone plays a permissive role since it regulates the calcium-influx into the cells and thus increases the vasoconstrictive effect. There is a positive correlation between parathormone and blood pressure, present in primary as well as secondary hyperparathyroidism. Moreover, patients with essential hypertension have high parathormone levels already before hypertension is diagnosed. A calcium-rich diet (> 1000 mg calcium daily) slightly decreases blood pressure. This positive effect is due to parathormone suppression with a subsequently decreased calcium content in the vascular smooth muscle cells. A calcium-rich diet inhibits lipogenesis in the fat tissue; thus additionally improving the cardiovascular risk profile.

Endovascular stenting of a renal transplant vein.

We describe successful endovascular stenting of a high-grade stenosis of a renal transplant vein in a 53-year old patient. Kidney transplantation had been performed due to IgA nephropathy and the patient had become symptomatic two months after uneventful recovery from operation.

[Urinary hormone analysis]. / Hormonanalysen im Urin.

Urinary hormone analysis is applied to detect an altered steroid hormone metabolism, an elevated production of biogenic amines and to non-invasively determine the protein hormone human beta-choriogonadotropin indicating a pregnancy. Occasionally, these determinations need to be complemented by plasma- or serum hormone analysis. Clinical data including current drug therapy and urinary creatinine as reference are required to interpret any urine analysis. Diseases to be investigated by steroid hormone analysis are excess production of a typical or atypical mineralocorticoid active steroid hormones, the hormonal activity of adrenal or ovarian tumors, acne of unknown origin, hirsutism, a PCO-, an adrenogenital or a suspected Cushing syndrome. Biogenic amines should be determined in suspected secondary or refractory arterial hypertension, in case of pheochromocytoma- or paraganglioma-associated symptoms or if a serotonin-producing tumor is suspected. In children genetically determined diseases are the primary background to perform an analysis.

Maternal Serum Lipid, Estradiol, and Progesterone Levels in Pregnancy, and the Impact of Placental and Hepatic Pathologies.

OBJECTIVE: Lipids and steroid hormones are closely linked. While cholesterol is the substrate for (placental) steroid hormone synthesis, steroid hormones regulate hepatic lipid production. The aim of this study was to quantify circulating steroid hormones and lipid metabolites, and to characterize their interactions in normal and pathological pregnancies with a focus on hepatic and placental pathologies. METHODS: A total of 216 serum samples were analyzed. Group A consisted of 32 patients with uncomplicated pregnancies who were analyzed at three different time-points in pregnancy (from the first through the third trimester) and once post partum. Group B consisted of 36 patients (24th to 42nd week of gestation) with pregnancy pathologies (IUGR n = 10, preeclampsia n = 13, HELLP n = 6, intrahepatic cholestasis n = 7) and 31 controls with uncomplicated pregnancies. Steroid profiles including estradiol, progesterone, and dehydroepiandrosterone were measured by GC-MS and compared with lipid concentrations. RESULTS: In Group A, cholesterol and triglycerides correlated positively with estradiol (cholesterol ρ = 0.50, triglycerides ρ = 0.57) and progesterone (ρ = 0.49, ρ = 0.53) and negatively with dehydroepiandrosterone (ρ = - 0.47, ρ = - 0.38). Smoking during pregnancy affected estradiol concentrations, leading to lower levels in the third trimester compared to non-smoking patients (p < 0.05). In Group B, cholesterol levels were found to be lower in IUGR pregnancies and in patients with HELLP syndrome compared to controls (p < 0.05). Steroid hormone concentrations of estradiol (p < 0.05) and progesterone (p < 0.01) were lower in pregnancies with IUGR. DISCUSSION: Lipid and steroid levels were affected most in IUGR pregnancies, while only minor changes in concentrations were observed for other pregnancy-related disorders. Each of the analyzed entities displayed specific changes. However, since the changes were most obvious in pregnancies complicated by IUGR and only minor changes were observed in pregnancies where patients had impaired liver function, our data suggests that placental rather than maternal hepatic function strongly determines lipid and steroid levels in pregnancy.

Prophylactic hemodialysis after radiocontrast media in patients with renal insufficiency is potentially harmful.

PURPOSE: Acute renal failure induced by contrast media is an important cause of hospital-acquired renal insufficiency. Preexisting renal failure and the dose of contrast media are known risk factors for the development of radiocontrast nephropathy. We performed a randomized trial to test whether radiocontrast nephropathy can be avoided by prophylactic hemodialysis immediately after the administration of contrast media in patients with impaired renal function. SUBJECTS AND METHODS: Renal function and other parameters, hemodialysis requirement, and relevant clinical events were recorded before and during the 6 days after administration of contrast media in 113 patients with a baseline serum creatinine level >200 microm/L (>2.3 mg/dL). Patients were randomly assigned to either hemodialysis (n = 55) or nonhemodialysis (n = 58) treatment after parenteral low-osmolality contrast media. RESULTS: The characteristics of the patients in the two groups were similar. Compared with baseline levels, the mean [+/- SD] serum creatinine level decreased at day 1 (277 +/- 95 microm/L), peaked at day 4 (353 +/- 126 microm/L), and returned to baseline at day 6 (327 +/- 119 microm/L, P <0.05 by analysis of variance) after administration of contrast media in the hemodialysis group, whereas in the nonhemodialysis group, no significant changes in mean serum creatinine level were observed. Eleven patients required 1 or more hemodialyses (8 in the hemodialysis group and 3 in the nonhemodialysis group, P = 0.12), 6 of whom (4 vs. 2, P = 0.44) required 3 or more hemodialyses. Clinically relevant events included pulmonary edema (1 vs. 4 patients, P = 0.36), myocardial infarction (2 vs. 2), stroke (2 vs. 0, P = 0.24), and death (1 vs. 1). CONCLUSIONS: The strategy of performing hemodialysis immediately after the administration of low-osmolality contrast media in all patients with a reduced renal function did not diminish the rate of complications, including radiocontrast nephropathy.

Altered nitric oxide production and exogenous nitric oxide do not affect the proliferation of rat mesangial cells.

OBJECTIVE: To examine the hypothesis that nitric oxide (NO) acts as an autocrine, antiproliferative regulator and that exogenous NO donor inhibitors the proliferation of cultured rat mesangial cells. DESIGN AND METHODS: The cellular effects of endogenous and exogenous NO were studied in rat mesangial cells in a two-dimensional culture of early mesangial cell passages. The proliferation of mesangial cells was determined by cell-counting and uptake of [3H]-thymidine. NO generation was induced by incubation with interleukin-1 beta (5 u/ml) or bacterial lipopolysaccharide (10 micrograms/ml) for 24 h. NO release by mesangial cells was assessed by measuring the accumulation of nitrite, the major stable end-product of NO, in mesangial cell supernates. In addition, cyclic GMP (cGMP) formation was measured by radioimmunoassay as an indicator for NO generation. RESULTS: The formation of nitrite and cGMP was significantly increased after incubation of mesangial cells with interleukin-1 beta or lipopolysaccharide. This effect was greatly reduced by an inhibitor of NO synthesis. NG-monomethyl-L-arginine (L-NMMA; 0.1 mmol/l). The NO donor 3-morpholino-sydnonimine-HCl also increased the cGMP concentrations in the mesangial cells. The proliferation of mesangial cells was analysed in growth-arrested and mitogen-stimulated (platelet-derived growth factor, platelet-derived growth factor plus ATP and fetal calf serum) mesangial cells in the presence and absence of L-NMMA and the NO synthase substrate L-arginine (1 mmol/l). At 48 h platelet-derived growth factor (50 ng/ml), and platelet-derived growth factor (50 ng/ml) plus ATP (0.1 mmol/l) and fetal calf serum 5% each significantly increased the uptake of [3H]-thymidine in mesangial cells. These effects were not altered in the presence of L-NMMA or L-arginine. Pretreatment with interleukin-1 beta or with lipopolysaccharide also failed to affect the uptake of [3H]-thymidine in resting or proliferating mesangial cells. 3-Morpholino-sydnonimine-HCl (10(-3) to 10(-6) mol/l) did not suppress the mitogen-induced proliferation of mesangial cells, even when it was administered three times a day. CONCLUSIONS: The present findings support recent observations that interleukin-1 beta and lipopolysaccharide strongly induce NO production in mesangial cells, as is shown indirectly by the greatly increased formation of nitrite and cGMP. However, these effects were not associated with antiproliferative action on mitogen-stimulated mesangial cells. Similarly, the exogenous NO donor 3-morpholino-sydnonimine-HCl induced cGMP formation but failed to inhibit proliferation of mesangial cells when used at a non-toxic dose. Our observations do not support the contention that the formation of NO and cGMP constitutes an autocrine downregulating mechanism in the control of the growth of mesangial cells. It remains to be seen what pathophysiological role the induction of NO release plays in the regulation of the behaviour of mesangial cells, e.g. during an inflammatory response to glomerular injury.

Sirolimus-associated eyelid edema in kidney transplant recipients.

BACKGROUND: The immunosuppressant sirolimus is effective in preventing acute rejection episodes. So far, unusual edema formation has not been reported as a side effect. METHODS: Two groups of patients with renal transplants, consisting of 11 patients each, were followed for up to 29 months. The immunosuppressive regimen was either sirolimus and prednisone with or without cyclosporine or azathioprine/mycophenolate and prednisone with cyclosporine. Routine follow-up included a thorough clinical investigation. Edema formation was documented photographically. RESULTS: In 5 of the 11 patients treated with sirolimus uni- or bilateral, non-itching, eyelid edema was observed. After discontinuation of sirolimus, lid edema disappeared. The duration until recovery varied from weeks to months. No cause of edema formation other than the treatment with sirolimus was detected. CONCLUSIONS: Severe eyelid edema formation seems to be associated with sirolimus treatment. The underlying mechanism is unknown.

Role of calcium in the progression of renal disease: experimental evidence.

Intracellular calcium mediates a wide array of cell functions in mesenchymal as well as in epithelial and endothelial cells. These comprise regulation of vascular tone, cell proliferation and synthesis of prostanoids and cytokines. Therefore, it is not surprising that a substantial body of evidence has emerged to suggest a crucial role of calcium in the initiation and perpetuation of renal disease. Increased deposition of calcium was found in the renal cortex of rats with remnant kidney and in kidney tissue of patients with end-stage renal failure. Calcium plays an important role in altered intrarenal and glomerular hemodynamics with increased glomerular wall tension as well as in cellular proliferation and in recurrent ischemic events leading to glomerulosclerosis and interstitial fibrosis. Besides hemodynamic mechanisms, additional calcium-dependent mechanisms must be considered for glomerular hypertrophy and/or mesangial proliferation to develop, namely the role of growth factors, prostanoids and cytokines. Their signals include receptor-regulated production of inositol-trisphosphate and diacylglycerol and the consecutive stimulation of protein kinase C and the Na/H-antiport. Full activation of this antiport, which raises intracellular pH and thereby stimulates protooncogenes, again requires the presence of calcium. Recurrent focal glomerular ischemia may result in cellular and mitochondrial calcium overload that may interfere with cellular energy metabolism. Calcium also activates proteinases and the production of oxidants to enhance neutrophil-mediated cell injury. These deleterious effects of calcium may initiate and perpetuate the progression of renal disease and eventually lead to end-stage renal failure.

Nitric oxide synthase activity and Doppler parameters in the fetoplacental and uteroplacental circulation in preeclampsia.

OBJECTIVE: We investigated the hypothesis that changes in blood flow in the uteroplacental and fetoplacental circulation in preeclampsia are associated with an abnormality of placental or uterine placental bed nitric oxide (NO) synthesis. METHODS: We measured pulsatility indices on Doppler waveform analysis from uterine and umbilical arteries in 20 patients with preeclampsia and 14 healthy pregnant controls before elective cesarean section. During cesarean section, biopsies from the uterine placental bed and the placenta were taken and the nitric oxide synthase (NOS) activity was measured by the [3H] L-arginine-[3H] L-citrulline conversion assay in these samples. RESULTS: The NOS activity was significantly lower in the uterine placental bed in comparison to the placental tissue (p < 0.01). Placental NOS activity was similar between patients with preeclampsia and healthy controls and in the groups with either a pathological or a normal Doppler flow in the umbilical artery. In the uterine placental bed however, NOS activity from patients with preeclampsia was significantly lower (p < 0.01), whereas the blood flow resistance in the uterine arteries was elevated (p < 0.01) in comparison to healthy controls. CONCLUSIONS: Our data show that pathological Doppler waveforms in the uterine arteries of patients with preeclampsia are paralleled by diminished NOS activity in the uterine placental bed. Therefore, the compromised NO production in the uterine placental bed may play an important role in the impaired uteroplacental blood flow and potentially in some pathological features of preeclampsia such as intervillous thrombosis formation and fetal growth retardation.

[Microhematuria--what next?]. / Mikrohämaturie--Wie weiter?

Asymptomatic microhematuria is a common reason for a urological consultation. Uncertainty prevails as to how meticulous the work-up must be, to not miss relevant or even life-threatening underlying diseases. To date, the Urological Associations have not released any guidelines to which extent patients need to be examined for asymptomatic microhematuria, which therefore is managed individually by each urologist. There are various potential examinations that can be applied, ranging from a clinical examination to a kidney biopsy. After reviewing the literature, an algorithm has been developed, which should assure diagnosis of serious disease and at the same time avoid costly, unpleasant and unnecessary examinations.

[Rhabdomyolysis]. / Rhabdomyolysen.

Rhabdomyolysis is a severe clinical symptom of variable etiology. Acquired factors of exogenous origin such as traumata and endogenous metabolic disturbances have to be separated from hereditary disease as causative mechanism. Most frequently, exertional stress during hyperthermia, traumatic damage or ethanol abuse are observed. Almost independent of the diverse initial events, the pathogenesis follows a common final pathway with intracellular calcium accumulation and ATP depletion. Clinical symptoms vary. Seldom, the classical triad of muscle pain, weakness, and dark urine is observed. Recurrent episodes should raise suspicion of an inherited disorder. Severe complications are hypovolemia, electrolyte disorders with hyperkalemia and hypocalcemia resulting in life threatening arrhythmias, a compartment syndrome, disseminated intravascular coagulation and acute renal failure, which is frequently oligo-anuric. In combination with often severe underlying disease, renal failure causes death in 1/5 of the patients. The diagnosis is made with the determination of serum creatine kinase and the myoglobin levels in plasma and urine. Therapeutic options are to correct the hypovolemia with sufficient fluid supply, the prevention of oliguria using loop diuretics, alkalinization of the urine, normalization of serum electrolytes with reduction of hyperkaemia, and decompression of compartment syndromes. An underlying disease should be evaluated to initiate specific therapeutical and preventative steps. Avoiding pre-disposing factors by identifying the mechanisms of disease will reduce the occurrence of rhabdomyolysis with its still high mortality.

[Edema in pregnancy--trivial?]. / Odeme in der Schwangerschaft--banal?

In pregnancy total body water increases. At least 25% of the fluid will be distributed to the interstitial space, ultimately clinically imposing as lower leg edema of pregnant women. Next to a cumulative sodium retention, altered local Starling forces and changes in the hydration of extracellular matrix add to the fluid shift. Edema have to be expected in most of the pregnant women and should not be used to diagnose preeclampsia. Atypical edema localization and local, unilateral edema should cast suspicion of other dangerous complications of pregnancy. Diuretics should be restricted to pulmonary edema of preeclampsia, but these drugs are not to be used to manage edema of pregnancy.

[Anuria after delivery]. / Anurie nach der Geburt.

During the last decade certain peripartal complications decreased dramatically in industrialized countries. Here, a case of a 27 years old Caucasian primagravida will be presented. In the presence of symptoms of a severe preeclamptic condition with signs of an impending HELP syndrome the patient underwent Caesarean section. Within hours following surgery she developed complete anuria. Nuclear magnetic resonance imaging and histological evaluation of a renal biopsy led to the diagnosis of an acute, bilateral renal cortical necrosis. Besides the preeclamptic condition no further underlying disease was present, in particular no hemolytic-uremic syndrome. Following progress made in modern perinatal management renal cortical necrosis almost disappeared. Yet, in the presence of this disease a significant maternal morbidity and mortality still remains.