About: Anuria is a research topic. Over the lifetime, 2445 publications have been published within this topic receiving 31489 citations. The topic is also known as: Anuria (context-dependent category) & Anuria (finding).
TL;DR: Evidence is provided that increases in peritoneal small-solute clearances within the range studied have a neutral effect on patient survival, even when the groups are stratified according to a variety of factors known to affect survival.
Abstract: Small-solute clearance targets for peritoneal dialysis (PD) have been based on the tacit assumption that peritoneal and renal clearances are equivalent and therefore additive. Although several studies have established that patient survival is directly correlated with renal clearances, there have been no randomized, controlled, interventional trials examining the effects of increases in peritoneal small-solute clearances on patient survival. A prospective, randomized, controlled, clinical trial was performed to study the effects of increased peritoneal small-solute clearances on clinical outcomes among patients with end-stage renal disease who were being treated with PD. A total of 965 subjects were randomly assigned to the intervention or control group (in a 1:1 ratio). Subjects in the control group continued to receive their preexisting PD prescriptions, which consisted of four daily exchanges with 2 L of standard PD solution. The subjects in the intervention group were treated with a modified prescription, to achieve a peritoneal creatinine clearance (pCrCl) of 60 L/wk per 1.73 m(2). The primary endpoint was death. The minimal follow-up period was 2 yr. The study groups were similar with respect to demographic characteristics, causes of renal disease, prevalence of coexisting conditions, residual renal function, peritoneal clearances before intervention, hematocrit values, and multiple indicators of nutritional status. In the control group, peritoneal creatinine clearance (pCrCl) and peritoneal urea clearance (Kt/V) values remained constant for the duration of the study. In the intervention group, pCrCl and peritoneal Kt/V values predictably increased and remained separated from the values for the control group for the entire duration of the study (P < 0.01). Patient survival was similar for the control and intervention groups in an intent-to-treat analysis, with a relative risk of death (intervention/control) of 1.00 [95% confidence interval (CI), 0.80 to 1.24]. Overall, the control group exhibited a 1-yr survival of 85.5% (CI, 82.2 to 88.7%) and a 2-yr survival of 68.3% (CI, 64.2 to 72.9%). Similarly, the intervention group exhibited a 1-yr survival of 83.9% (CI, 80.6 to 87.2%) and a 2-yr survival of 69.3% (CI, 65.1 to 73.6%). An as-treated analysis revealed similar results (overall relative risk = 0.93; CI, 0.71 to 1.22; P = 0.6121). Mortality rates for the two groups remained similar even after adjustment for factors known to be associated with survival for patients undergoing PD (e.g., age, diabetes mellitus, serum albumin levels, normalized protein equivalent of total nitrogen appearance, and anuria). This study provides evidence that increases in peritoneal small-solute clearances within the range studied have a neutral effect on patient survival, even when the groups are stratified according to a variety of factors (age, diabetes mellitus, serum albumin levels, normalized protein equivalent of total nitrogen appearance, and anuria) known to affect survival. No clear survival advantage was obtained with increases in peritoneal small-solute clearances within the range achieved in this study.
TL;DR: Surgical decompression of the abdomen improved oxygenation, ventilation, cardiac output, atrial filling pressures, and urine output within 15 min, and the cardiovascular effects of massively elevated IAP compounded by the requisite supportive care may require surgical relief.
Abstract: Massive elevation of intra-abdominal pressure (IAP) causes cardiovascular, respiratory, and renal dysfunction. We managed eight patients with high IAP (mean 51 +/- 7 cm H2O), six of whom had hemodynamic measurements; a clinical syndrome, characterized by hemodynamic, respiratory, and renal dysfunction, then became apparent. We report a) a baseline cardiopulmonary profile and response to an acute vascular volume challenge in six patients and b) surgical decompression of the abdomen in four patients. The clinical impression of hypovolemia was confused by small to normal left ventricular end-diastolic volume (64 +/- 14 ml) and normal ejection fraction (55 +/- 6%) despite very high right and left atrial filling pressures. Complete ventilatory support was necessary to maintain oxygenation and ventilation; oliguria (urine output less than 10 ml/h) was present. Pericardial effusion was absent. After fluid challenge (10 ml/kg of colloid or crystalloid infused iv over 10 min), filling pressures, cardiac output, and stroke volume all increased significantly (p less than .025) while heart rate decreased. Surgical decompression of the abdomen improved oxygenation, ventilation, cardiac output, atrial filling pressures, and urine output within 15 min. The cardiovascular effects of massively elevated IAP compounded by the requisite supportive care may require surgical relief.
TL;DR: In this paper, kidney biopsy was performed immediately post-mortem in consecutive patients who died of septic shock and the results showed that acute tubular lesion intensity correlated with blood lactate concentration; intense infiltration by leukocytes, mainly monocytic, in glomeruli and interstitial capillaries; presence of tubular cell apoptosis proved by the presence of apoptotic bodies significantly more frequently than in controls and confirmed by TUNEL and activated caspase-3 staining.
Abstract: Septic shock is one of the leading causes of acute kidney injury. The mechanisms of this injury remain mostly unknown notably because of the lack of data on renal histological lesions in humans. Kidney biopsy was performed immediately post-mortem in consecutive patients who died of septic shock. Comparisons were made with specimens from eight patients who died of trauma on scene and nine ICU patients that died of non-septic causes. Nineteen septic patients were included, 11 were male, and age was 72 ± 12 years. Anuria occurred in all patients 2.2 ± 1.4 days before death. Seven patients had disseminated intravascular coagulation. In all patients we observed (1) acute tubular lesions whose intensity correlated with blood lactate concentration; (2) intense infiltration by leukocytes, mainly monocytic, in glomeruli and interstitial capillaries as compared to controls; (3) presence of tubular cell apoptosis proved by the presence of apoptotic bodies (2.9% of tubular cells) significantly more frequently than in controls and confirmed by TUNEL and activated caspase-3 staining. Arteriolar/arterial thromboses were observed in only 4 of 19 patients, without any association with presence of disseminated intravascular coagulation. Kidney lesions in septic shock go beyond those associated with simple acute tubular injury, notably capillary leukocytic infiltration and apoptosis. Vascular thrombosis, however, did not appear to play a major role in the majority of patients. The extent to which these lesions are specific to sepsis or are common to all multi-organ failure independent of its cause is yet to be elucidated.
TL;DR: It is proposed that renal lesions and early anuria result from chronic low perfusion pressure of the fetal kidney, a consequence of renin-angiotensin system inactivity, the first identification to the authors' knowledge of a renal mendelian disorder linked to genetic defects in the renin
Abstract: Autosomal recessive renal tubular dysgenesis is a severe disorder of renal tubular development characterized by persistent fetal anuria and perinatal death, probably due to pulmonary hypoplasia from early-onset oligohydramnios (Potter phenotype). Absence or paucity of differentiated proximal tubules is the histopathological hallmark of the disease and may be associated with skull ossification defects. We studied 11 individuals with renal tubular dysgenesis, belonging to nine families, and found that they had homozygous or compound heterozygous mutations in the genes encoding renin, angiotensinogen, angiotensin converting enzyme or angiotensin II receptor type 1. We propose that renal lesions and early anuria result from chronic low perfusion pressure of the fetal kidney, a consequence of renin-angiotensin system inactivity. This is the first identification to our knowledge of a renal mendelian disorder linked to genetic defects in the renin-angiotensin system, highlighting the crucial role of the renin-angiotensin system in human kidney development.
TL;DR: This open-label randomized trial in patients receiving peritoneal dialysis showed that ramipril reduced declines in glomerular filtration rate and decreased the hazard rate of anuria at 1 year, and several trials have shown that ACE inhibitors reduce the rates of renal function deterioration in patients with diabetic nephropathy.
Abstract: Background Residual renal function is an important determinant of mortality and morbidity in patients receiving peritoneal dialysis. However, few studies have evaluated therapeutic approaches for preserving residual renal function after the initiation of dialysis. Objective To test the hypothesis that the angiotensin-converting enzyme (ACE) inhibitor ramipril slows the decline in residual renal function in patients with end-stage renal failure treated with peritoneal dialysis. Design Randomized, open-label, controlled trial. Setting Single-center study in the dialysis unit of a university teaching hospital. Patients 60 patients receiving peritoneal dialysis. Measurements Patients were randomly assigned to ramipril (5 mg daily) or no treatment. The target blood pressure was 135/85 mm Hg or less. Rate of decline in residual glomerular filtration rate (GFR) and development of complete anuria were compared among groups. Results Over 12 months, average residual GFR declined by 2.07 mL/min per 1.73 m2 in the ramipril group versus 3.00 mL/min per 1.73 m2 in the control group (P = 0.03). The difference between the average changes in residual GFR in the ramipril and control groups from baseline to 12 months was 0.93 mL/min per 1.73 m2 (95% CI, 0.09 to 1.78 mL/min per 1.73 m2). At 12 months, 14 patients in the ramipril group and 22 in the control group developed anuria. With intention-to-treat multivariable analysis using the Cox model, it was estimated that at 3, 6, and 9 months, patients assigned to ramipril had a higher adjusted hazard of complete anuria than did patients assigned to no treatment. Of the 25 patients who still did not have complete anuria at 12 months, those assigned to ramipril had a better prognosis than did those assigned to no treatment (adjusted hazard ratio, 0.58 [CI, 0.36 to 0.94]). The rates of death from any cause, duration of hospitalization, and cardiovascular events did not differ significantly between groups. Conclusions Although the trial was small and had a limited ability to exclude effects of potential confounding factors, the angiotensin-converting enzyme inhibitor ramipril may reduce the rate of decline of residual renal function in patients with end-stage renal failure treated with peritoneal dialysis.