Search

Old age was identified as a strong risk factor for acute kidney injury (AKI). Our objectives were to provide estimates of AKI, risk factors and outcomes in patients ≥ 75 years for whom data are scarce.Observational studies and randomized controlled trials between 2005 and 2021 with patients of mean or median age ≥ 75 years, reporting AKI according to current definitions. Data on AKI incidence, risk factors and mortality were analyzed separately in unselected (UC) and acute heart failure (AHF) cohorts.Twenty-six observational studies and 4 randomized controlled trials with 51,111 UC and 25,414 AHF patients were included. Ages averaged 79.4 and 79.8 years, respectively. Pooled risk ratios (RRs) of AKI rates were 26.29% (95% confidence intervals (CI) 13.20-41.97) (UC) and 24.21% (95% CI 20.03-28.65) (AHF). In both cohorts, AKI was associated with decreased estimated glomerular filtration rate at baseline, chronic kidney disease (UC: RR 1.80 (95% CI 1.15-2.80), AHF: RR 1.51 (95% CI 1.26-1.95) and hypertension (UC: RR 1.30 (95% CI 1.09-1.56), AHF: RR 1.07 (95% CI 1.05-1.09). RRs of AKI in patients on renin-angiotensin-inhibitors were 0.87 (95% CI 0.78-0.97) and 0.88 (95% CI 0.78-0.98) in UC and AHF, respectively. AKI was consistently associated with increased risk of in-hospital mortality (UC: RR 3.15 (95% CI 2.28-4.35), AHF: RR 4.28 (95% CI 2.53-7.24).AKI is frequent in patients ≥ 75 years. While reduced renal function at baseline, CKD and hypertension were associated with AKI development, renin-angiotensin-inhibitors may be protective. Older AKI patients showed higher short-term mortality rates.

in press

Hintergrund In Deutschland leben ungefahr 800.000 Menschen in Pflegeeinrichtungen. Die arztliche Versorgung erfolgt durch ambulant tatige Haus- und Facharzte. Wahrend nahezu alle Bewohner regelmasigen Kontakt zu Hausarzten haben, gilt dies fur andere Facharztgruppen nur in unterschiedlichem Ausmas.

Background Acute kidney injury (AKI) is a prominent problem in hospitalized patients and associated with increased morbidity and mortality. Clinical medicine is currently hampered by the lack of accurate and early biomarkers for diagnosis of AKI and the evaluation of the severity of the disease. In 2010, we established a multivariate peptide marker pattern consisting of 20 naturally occurring urinary peptides to screen patients for early signs of renal failure. The current study now aims to evaluate if, in a different study population and potentially various AKI causes, AKI can be detected early and accurately by proteome analysis. Methods Urine samples from 60 patients who developed AKI after cardiac surgery were analyzed by capillary electrophoresis-mass spectrometry (CE-MS). The obtained peptide profiles were screened by the AKI peptide marker panel for early signs of AKI. Accuracy of the proteomic model in this patient collective was compared to that based on urinary neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) ELISA levels. Sixty patients who did not develop AKI served as negative controls. Results From the 120 patients, 110 were successfully analyzed by CE-MS (59 with AKI, 51 controls). Application of the AKI panel demonstrated an AUC in receiver operating characteristics (ROC) analysis of 0.81 (95 % confidence interval: 0.72–0.88). Compared to the proteomic model, ROC analysis revealed poorer classification accuracy of NGAL and KIM-1 with the respective AUC values being outside the statistical significant range (0.63 for NGAL and 0.57 for KIM-1). Conclusions This study gives further proof for the general applicability of our proteomic multimarker model for early and accurate prediction of AKI irrespective of its underlying disease cause. Electronic supplementary material The online version of this article (doi:10.1186/s13054-016-1344-z) contains supplementary material, which is available to authorized users.

Das akute Nierenversagen (ANV) tritt, nach der aktuell entwickelten Definition, mit einer Inzidenz von bis zu 30% nach kardiochirurgischen Eingriffen auf, bei etwa 1% der Betroffenen als dialysepflichtiges Nierenversagen, weshalb der Begriff „cardiac surgery associated acute kidney injury“ (CSA AKI) gepragt wurde. Die ANV-assoziierte Mortalitat liegt zwischen 15 und 30% und CSA AKI erhoht die Mortalitat, unabhangig von der Komorbiditat. Lediglich bei 50% der Uberlebenden kommt es zur vollkommenen Regeneration der Nierenfunktion. Die Pathophysiologie des CSA AKI ist keineswegs auf den Einsatz der extrakorporalen Zirkulation begrenzt, sondern ausgesprochen komplex und multifaktoriell und beinhaltet v. a. endogene und exogene Nephrotoxine, Inflammation, Hypoperfusion sowie metabolische und neurohormonale Faktoren. Es existiert keine kausale Therapie des CSA AKI; extrakorporale Nierenersatzverfahren stellen lediglich eine supportive Therapie des ANV dar, um die Zeit bis zur renalen Regeneration zu uberbrucken. Daher kommt der primaren und sekundaren Pravention des ANV mit Korrektur aller vermeidbaren und modifizierbaren Risikofaktoren die entscheidende Rolle zu.

Multiple myeloma (MM) is frequently complicated by renal insufficiency, which is associated with an unfavorable prognosis. Serum cystatin C is a new and accurate marker of glomerular filtration rate. Global gene expression analysis has revealed serum cystatin C as one of the most highly upregulated genes in MM. Recent data have shown serum cystatin C as an independent prognostic marker in MM. To further elucidate the prognostic significance of serum cystatin C, we investigated pretreatment serum cystatin C levels in 68 newly diagnosed patients homogeneously treated with high-dose melphalan followed by autologous stem cell transplantation. Median serum cystatin C level in MM patients was significantly higher than in the 66 healthy controls (1.07 vs. 0.74 mg/L [p = 0.002]). Median serum cystatin C levels significantly increased with higher International Staging System (ISS) stages (stage I 0.72 mg/L; stage II 0.89 mg/L; stage III 1.28 mg/L; p < 0.0001). Higher serum cystatin C was positively correlated with higher serum levels of creatinine (r = 0.84; p < 0.0001), β2-microglobulin (r = 0.72; p < 0.0001), LDH (r = 0.43; p = 0.0003), white blood cell counts (r = 0.61; p < 0.0001) and calcium (r = 0.29; p = 0.016), and negatively correlated with lower serum albumin levels (r = 0.44; p < 0.0001) and hemoglobin levels (r = 0.31; p = 0.01). Using ROC analysis, patients with serum cystatin C levels ≥0.95 mg/L (n = 24) had a significantly shorter event-free survival (EFS) and overall survival (OS) than patients with serum cystatin C levels

Peritoneal- und Hamodialyse werden als unterschiedliche, aber gleichwertige Dialyseverfahren angesehen. Fur die meisten Patienten sind aus medizinischer Sicht beide Verfahren gleichermasen geeignet. Wichtig fur die Auswahl ist der Wunsch des umfassend informierten Patienten. Die durch die Peritonealdialyse erreichten Moglichkeiten der Berufsausubung, Freizeitgestaltung, Reiseplanung und Unabhangigkeit haben fur viele Patienten einen hohen Stellenwert. Die Peritonealdialyse ist fur Kinder und fur Patienten mit Problemen mit der Hamodialyse zu bevorzugen und kontraindiziert bei aktiver oder intermittierender Divertikulitis. Erschwerte Bedingungen fur die Peritonealdialyse sind Erkrankungen mit erhohtem Peritonitisrisiko, Hernien, schwere obstruktive Lungenerkrankung, ausgepragter Eiweismangel und schwere Psychose. Falschlich angenommene Kontraindikationen sind Multimorbiditat, fortgeschrittenes Lebensalter, kardiovaskulare Erkrankungen, Transplantatversagen, Zystennieren und Anurie.

Although the role of plasmapheresis in liver failure is not clearly established yet, encouraging reports have addressed its efficacy in the setting of resections for primary liver malignancies, small-for-size syndrome after live donor liver transplantation, and acute liver failure. However, we have not encountered any literature reports of successful treatment of postoperative liver failure after resection of metastatic lesions where effect of the earlier tumor dissemination remains unclear. We would like to describe the case of a 56-year-old man who underwent a low anterior resection for rectal adenocarcinoma pT2 N0 M1 (liver) G1-2 in May 2004. Lymph nodes were negative, and there were no pulmonary metastases. The liver lesion was treated with one session of radiofrequency ablation and 2 courses of transarterial chemoembolizations. He also received repeated cycles of systemic chemotherapy, initially with 5-flurouracil/leucovorin and more recently with capecitabine/oxaliplatin. In March 2006, approximately 2 years after the low anterior resection, he presented to undergo resection of the 11 cm solitary liver metastasis, localized in segment VIII, with involvement of both right and middle hepatic veins. During preoperative planning, the volume of segments I, II, and III was calculated to be approximately 420 ml and considered adequate for his BMI of 26. At the time of the intervention, there were no macroscopic sings of cirrhosis or steatosis. We performed a right trisectionectomy (segments IV–VIII), with partial resection of the diaphragm, hilar lymphadenectomy, portal vein resection and reconstruction, cholecystectomy, and insertion of a T-tube. Histological exam showed a G2–3 colorectal metastasis, with areas of tumor necrosis, and liver parenchyma characterized by 25% steato-hepatitis. Postoperatively, he developed liver insufficiency with bilirubin levels as high as 42 mg/dl, and multi-organ failure requiring high doses of vasopressors, mechanical ventilation, and continuous venovenous hemodialysis. Our treatment consisted of a total of nine consecutive sessions of plasmapheresis, starting on the first postoperative day. The patient gradually recovered, and was discharged from the hospital on postoperative day 47. He is currently alive and well, with normal liver function and no evidence of tumor recurrence 12 months postoperatively. The presence of vascular and steatotic changes in patients treated with chemotherapy can be a source of morbidity and mortality at the time of surgical resection of liver metastases. However, the documented 25% steatohepatitis in our case can not be definitively characterized as a chemotherapy associated one, since our patient had a BMI of 26 before liver resection. We hope this report will provide useful additional information on the short and long term effects of plasmapharesis, especially as supportive procedure after major hepatectomy, in the current setting of increasingly aggressive chemotherapy treatments. Int J Colorectal Dis (2008) 23:553 DOI 10.1007/s00384-007-0405-9

In our review, we stated that C-reactive protein (CRP) levels were not adjusted for in the Cardiovascular Health Study. As can be seen from the legend for Table 1 of our paper, CRP was well included in the various analyses published from the Cardiovascular Health Study data.

Sirs, In a recent publication in Pediatic Nephrology Hellerstein et al. [1] proposed the urinary cystatin C/creatinine ratio as a marker of glomerular filtration rate (GFR). However appealing the idea of screening urine to detect probands with decreased GFR may be, some words of caution are warranted. The patient population of Hellerstein et al. was comprised mostly of patients with tubulointerstitial damage from uropathies. Unfortunately, two groups that are critical for the evaluation of their technique were barely studied. These include patients with isolated tubular injury who have a high urinary cystatin C/creatinine ratio but normal GFR [2, 3] and patients with minimal change nephrotic syndrome. The authors present one single patient with IgA nephropathy with nephrotic-range proteinuria and a high urinary cystatin C/creatinine ratio but fail to state the GFR. Data both in rats [4] and in man [5] indicate that in nephrotic syndrome albumin competes with low molecular weight protein absorption in the proximal tubule [5], leading to low molecular weight proteinuria. Therefore the cystatin C/creatinine ratio may well be an indicator of renal disease but it does not reliably reflect GFR in situations where there is significant proteinuria of tubular or glomerular origin. The authors assess the analytical performance of the urinary cystatin C/creatinine ratio using a GFR cut-off of 60 ml/min per 1.73 m. Although the non-invasiveness of their method is appealing for screening purposes, such a low threshold would miss children in the “creatinineblind” range who should be the target group of screening programs for renal disease. Thus detection of incipient renal impairment remains the preserve of serum cystatin C [6], which cannot be replaced by the less invasive urinary test proposed by the authors.