Cause Of Renal Failure Research Articles

Selective Bilirubin Removal as Treatment of Jaundice-Related Kidney Injury

Severe hyperbilirubinemia is often associated with acute kidney injury (AKT). Considering the potential renal toxicity of bilirubin, it is possible that bilirubin removal per se could represent a way to improve renal function in patients experiencing jaundice-related AKI. Here we present the case of a 47-year-old male patient, who was admitted due to severe jaundice and ascites. The patient presented a history of idiopathic myelofibrosis, associated with liver disease with stable bilirubin values of about 4 mg/dL. At admission, blood tests showed plasma bilirubin of 45 mg/dL, normal liver enzymes and AKI (creatinine 2.1 mg/dL vs a previous value of 0.7 mg/dL). Instrumental examinations and liver biopsy showed a picture of diffuse inflammatory cholangitis. During hospitalization, bilirubin levels further raised (up to 59.7 mg/dL) and, simultaneously, kidney function declined. We excluded functional causes of renal failure and hepatorenal syndrome and thus, suspecting a bilirubin-associated nephrotoxicity, we decided to treat the patient with plasma adsorption perfusion (PAP), a technique based on plasma adsorption by a bilirubin-specific adsorbent. After the treatment plasma bilirubin, as well as creatinine serum levels, progressively decreased. Unfortunately, about 10 days after the beginning of PAP the patient died of septic shock. This case represents an additional proof of the potential nephrotoxicity of bilirubin, suggesting that PAP could be a valuable therapeutic option in patients with jaundice-related AKI.

Slit2 Prevents Neutrophil Recruitment and Renal Ischemia-Reperfusion Injury

Neutrophils recruited to the postischemic kidney contribute to the pathogenesis of ischemia-reperfusion injury (IRI), which is the most common cause of renal failure among hospitalized patients. The Slit family of secreted proteins inhibits chemotaxis of leukocytes by preventing activation of Rho-family GTPases, suggesting that members of this family might modulate the recruitment of neutrophils and the resulting IRI. Here, in static and microfluidic shear assays, Slit2 inhibited multiple steps required for the infiltration of neutrophils into tissue. Specifically, Slit2 blocked the capture and firm adhesion of human neutrophils to inflamed vascular endothelial barriers as well as their subsequent transmigration. To examine whether these observations were relevant to renal IRI, we administered Slit2 to mice before bilateral clamping of the renal pedicles. Assessed at 18 hours after reperfusion, Slit2 significantly inhibited renal tubular necrosis, neutrophil and macrophage infiltration, and rise in plasma creatinine. In vitro, Slit2 did not impair the protective functions of neutrophils, including phagocytosis and superoxide production, and did not inhibit neutrophils from killing the extracellular pathogen Staphylococcus aureus. In vivo, administration of Slit2 did not attenuate neutrophil recruitment or bacterial clearance in mice with ascending Escherichia coli urinary tract infections and did not increase the bacterial load in the livers of mice infected with the intracellular pathogen Listeria monocytogenes. Collectively, these results suggest that Slit2 may hold promise as a strategy to combat renal IRI without compromising the protective innate immune response.

Proteinuria and its relation to diverse biomarkers and body mass index in chronic hemodialysis

BackgroundCertain adipokines exert direct effects on proteinuria, a cardiovascular risk factor ignored in hemodialysis. We measured different adipokines according to body mass index (BMI) in relation to proteinuria.MethodsPatients numbered 57: group A (GA), BMI<25, n = 22; GB, BMI 25–30, n = 15; and GC, BMI > 30, n = 20. There were no statistical differences in age, sex, time on dialysis, cause of renal failure, diabetes, hypertension, C-reactive protein, or nutritional status. Measures were taken of 24-hour diuresis and proteinuria, ultrafltration, albumin, pro-brain natriuretic peptide (Pro-BNP), insulin, adiponectin, leptin, and ghrelin.ResultsProteinuria was signifcantly higher in GC versus (vs) GA (1.5 g/day, range 0.30–14 vs 0.72 g/day, range 0.1–2.7; P < 0.01) and correlated signifcantly with leptin levels (ρ = 0.47, P < 0.05). In GA, elevated levels of Pro-BNP, adiponectin, and ghrelin were associated with lower degrees of proteinuria. Signifcant correlations were found between adiponectin and leptin (ρ = −0.54, P = 0.03), and adiponectin and Pro-BNP (ρ = 0.59, P = 0.02). Though not signifcant, there were more diabetics in GC (GA four, GB three, GC ten). As BMI increased in GB and GC, Pro-BNP, adiponectin, and ghrelin levels decreased signifcantly, while proteinuria, insulin, and homeostasis model assessment of insulin resistance increased. Leptin levels were signifcantly elevated in GC vs GA and GB. In GC, ghrelin correlated signifcantly with Pro-BNP (ρ = 0.51, P = 0.03), while leptin correlation with Pro-BNP was inverse and signifcant in GA (ρ = −0.74, P < 0.001) and inverse and nonsignifcant in GB and GC.ConclusionIn patients with BMI < 25, higher adiponectin, ghrelin, and Pro-BNP levels were associated with lower proteinuria and leptinemia. In obesity, hyperleptinemia and hyperinsulinemia associated with higher proteinuria; whether decreased adiponectin–ghrelin–ProBNP and/or elevated leptin–insulin levels aggravate proteinuria remains to be determined.

G69(P) Paediatric Renal Transplantation with Bardet-Biedl Syndrome (BBS) and Situs Inversus Totalis

IntroductionBardet-Biedl syndrome (BBS) is a rare autosomal recessive disorder characterised by a genetic dysfunction that causes cystic malformation of the kidneys alongside features such as postaxial polydactyly, central obesity and...

Urine miRNAs: Potential biomarkers for monitoring progression of early stages of diabetic nephropathy

With a steep increase in the incidence of type 1 and 2 diabetes globally, diabetic nephropathy (DN) has now become the leading cause of renal failure in the world. There are no suitable biomarkers for the diagnosis of early stages of DN. In recent years, tremendous efforts are being made worldwide to delineate the role of micro RNAs in the pathogenesis of DN. Circulating miRNAs in serum, plasma, urine and other body fluids, which reflect a response to various pathophysiological stresses, are being investigated in the context of diabetic nephropathy. Delineation of the changes in miRNA levels in patients with DN may lead to a better understanding of the progression of the disease. We present here an exhaustive survey of the miRNA literature, highlighting various studies performed over the last decade. The aim is to assess if changes in various miRNAs could correlate with the progression of diabetic nephropathy. Based on the survey, we found that miRNA-377, miRNA-192, miRNA-216/217 and miRNA-144 are increased in body fluids of patients with DN, while miRNA-21 and miRNA-375 are decreased. Overall, there are a very few miRNAs that are kidney specific, and although significant differences were observed in the urinary excretion of certain miRNAs, they were not correlative to their levels in the blood or plasma. Thus, it is completely plausible that urine-specific miRNAs could serve as novel biomarkers for the diagnosis of early stages of diabetic nephropathy.

NPHP4 mutation is linked to cerebello‐oculo‐renal syndrome and male infertility

Nephronophthisis is the most common genetic cause of renal failure in children and young adults. It is genetically heterogeneous and can be seen in isolation or in combination with other ciliopathy phenotypes. Here we report an index case where nephronophthisis is associated with oculomotor apraxia and cerebellar abnormalities, consistent with the clinical diagnosis of cerebello-oculo-renal syndrome. Prompted by a family history of an uncle with early onset end stage renal failure and infertility, we performed semen analysis on the index. This revealed marked reduction in the count of motile sperms as well as multiple abnormalities in the head and tail. Autozygome-guided mutation analysis followed by exome sequencing and segregation analysis revealed a homozygous truncating mutation in NPHP4, indicating that mutations of this gene can on rare occasions cause cerebello-oculo-renal syndrome. Our finding of severe male infertility in a family with NPHP4 truncation is strongly supported by the mouse model and, to our knowledge, is the first reported male infertility phenotype in association with NPHP4 or any other nephrocystin in humans.

Diabetes is the Leading Cause of ESRD in Haemodialysis Patients

Diabetes is one of the leading causes of ESRD and the no of diabetes patients is increasing day by day.In the developed world it is the first and foremost cause of renal failure. However in the developing countries it has beenconsidered as second most common cause after GN.This study was a cross sectional study conducted during Oct 2010 to Sept 2011, in the dept of Nephrology, Dhaka Medical College and Hospital to determine the cause of renal failure with specific object to find out the leading cause of ESRD among the Haemodialysis patients. This study found Diabetes as the leading cause of ESRD accounting 44.1% of whole population.DOI: http://dx.doi.org/10.3329/jom.v14i1.14595 J MEDICINE 2013; 14 : 62-64

Unrecognized anterior urethral valves as a cause of renal failure

Abstract Congenital obstruction of the male urethra is usually caused by posterior urethral valves. Anterior urethral valves (AUV) represent a rare anomaly with a wide spectrum of presentation varying from mild voiding difficulties to end-stage renal disease. Prompt diagnosis and appropriate treatment is essential to prevent renal impairment. We report the case of a 13 month-old boy who presented with deterioration of kidney function caused by unrecognized AUV disorder. Temporary cutaneous vesicostomy was necessary to protect the upper urinary tract from further damage and to stabilize renal function. Even though a voiding cystourethrogram (VCUG) demonstrated obstruction of distal urethra, AUV were initially overlooked but finally diagnosed on additional VCUG followed by urethroscopy.

Association between a TGFBR2 Gene Polymorphism (rs2228048, Asn389Asn) and Acute Rejection in Korean Kidney Transplantation Recipients

Transforming growth factor-β (TGF-β) signaling transduction initiates TGF-β activation, resulting in activation of TGF-β receptor II (TGFBR2). Any quantitative and qualitative changes in TGFBR2 are expected to affect the TGF-β signaling pathway, which occupies a central position with respect to the regulation of cell growth, differentiation, apoptosis, immune reaction, angiogenesis and extracellular matrix formation. Recent studies have shown that TGF-β1 gene polymorphisms may confer susceptibility to early acute and chronic allograft rejection in kidney transplantation recipients. In this study, we assessed whether polymorphisms of the TGFBR2 gene were associated with susceptibility to kidney transplantation rejection. A total of 347 renal allograft recipients transplanted at three centers in Korea were analyzed. Three SNPs (rs764522, rs3087465, rs2228048) of the TGFBR2 gene were genotyped from genomic DNA with direct sequencing. Multiple logistic regression models (codominant, dominant, recessive, and log-additive) were performed to evaluate odds ratios (ORs), 95% confidence intervals (CIs), and p-values. A total of 63 patients (18%) developed acute rejection (AR). There were no significant differences in age, sex, number of HLA mismatches, cause of renal failure, or immunosuppressant regimen between the AR and non-AR group. The synonymous SNP rs2228048 was significantly associated with AR (p = 0.020 in recessive model, and p = 0.036 in log-additive model. The allele frequencies of rs2228048 were different between the AR and non-AR group (p = 0.026). These results suggest that the synonymous TGFBR2 gene SNP rs2228048 may be associated with the development of AR in Korean kidney transplantation recipients.Authors Yeong-Hoon Kim and Tae Hee Kim contributed equally to this work and are considered co-first authors.

Are Killer Cell Immunoglobulin-Like Receptor Genes Important for the Prediction of Kidney Graft Rejection?

Killer cell immunoglobulin-like receptors (KIRs) are expressed on natural killer cells and minor subpopulations of thymus-derived (T) lymphocytes. KIRs may have a long cytoplasmic tail and inhibit cell activation upon ligand (HLA class I) binding, or they may have a short cytoplasmic tail and activate a cell after ligand binding. They are encoded by up to 14 genes present in different individuals in different combinations, whence their associations with several human diseases. KIR involvement in the fate of kidney allograft has not been extensively studied; nevertheless some associations had already been noticed. Their results are not concordant: some authors found no effect of KIR genotype, whereas others detected protective effect of KIR2DL2/KIR2DS2 or KIR-KIR ligand mismatch. We found an association of KIR2DS4 gene with acute rejection and a protective effect of KIR2DS5 gene. Interestingly, in patients, whose end-stage renal disease was caused by glomerulonephritis, the effect of KIR2DS4 was stronger than HLA mismatch, whereas opposite was true for recipients with other causes of renal failure.

Severe Prenatal Renal Anomalies Associated with Mutations in HNF1B or PAX2 Genes

Congenital anomalies of the kidney and urinary tract (CAKUT) are a frequent cause of renal failure in children, and their detection in utero is now common with fetal screening ultrasonography. The clinical course of CAKUT detected before birth is very heterogeneous and depends on the level of nephron reduction. The most severe forms cause life-threatening renal failure, leading to perinatal death or the need for very early renal replacement therapy. This study reports the screening of two genes (HNF1B and PAX2) involved in monogenic syndromic CAKUT in a cohort of 103 fetuses from 91 families with very severe CAKUT that appeared isolated by fetal ultrasound examination and led to termination of pregnancy. This study identified a disease-causing mutation in HNF1B in 12 cases from 11 families and a mutation in PAX2 in 4 unrelated cases. Various renal phenotypes were observed, but no case of bilateral agenesis was associated with HNF1B or PAX2 mutations. Autopsy identified extrarenal abnormalities not detected by ultrasonography in eight cases but confirmed the absence of extrarenal defects in eight other cases. A positive family history of renal disease was not significantly more frequent in cases with an identified mutation. Moreover, in cases with an inherited mutation, there was a great phenotypic variability regarding the severity of the renal disease within a single family. Our results suggest that mutations in genes involved in syndromic CAKUT with Mendelian inheritance are not rare in fetal cases with severe CAKUT appearing isolated at prenatal ultrasound, a finding of clinical importance because of genetic counseling.

Associations of marital status with mortality from all causes and mortality from cardiovascular disease in Japanese haemodialysis patients

Marital status is an important social factor associated with increased mortality from cardiovascular disease (CVD) and all causes. However, there has been no study on the association of marital status with mortality in haemodialysis patients. We analysed data from a 5-year prospective cohort study of 1064 Japanese haemodialysis patients aged 30 years or older. Marital status was classified into three groups: married, single and divorced/widowed. Cox's regression was used to estimate multivariate hazard ratios (HRs) [95% confidence intervals (CIs)] for all-cause mortality and CVD mortality according to marital status after adjusting for age, sex, duration of haemodialysis, cause of renal failure, body mass index, systolic blood pressure, total cholesterol, high density lipoprotein-cholesterol, albumin, high-sensitivity C-reactive protein, co-morbid conditions, smoking, alcohol consumption, education levels and job status. Single patients had higher risks than married patients for mortality from all causes (HR = 1.51, 95% CI: 1.06-2.16) and mortality from CVD (HR = 1.68, 95% CI: 1.03-2.76), and divorced/widowed patients had a higher risk than married patients for mortality from CVD (HR = 1.73, 95% CI: 1.15-2.60). After stratification by age, single patients aged 30-59 years had significantly higher risks for all-cause mortality and CVD mortality. The findings suggest that single status is a significant predictor for all-cause mortality and CVD mortality and that divorced/widowed status is a significant predictor for CVD mortality in haemodialysis patients.

Early Experience with a Newly Developed Electrospun Polycarbonate-urethane Vascular Graft for Hemodialysis Access

In this pilot study, we tested a newly developed electrospun multilayered, self-sealing graft, AVflo™, specifically designed for early hemodialysis access. Ten eligible consenting patients had a polycarbonate-urethane graft (AVflo™) implanted and were followed up prospectively for at least six months. Performance measures included graft patency, complications and time to first cannulation. Mean age of the patients was 66.7 ± 10 years. Chronic glomerulonephritis was the most common cause of renal failure. A total of 70% of the patients had a history of previous vascular access and 40% history of minimally invasive radiologic procedures for patency maintenance. In 40% of the cases the need for AV graft implantation was because of recurrent infections from permanent catheter for dialysis. Seven grafts were placed in the upper arm and three in the thigh. Mean follow up was 230 ± 75 days. There were no systemic or local reactions to the graft and we did not report any graft infections. Two grafts thrombosed because of severe bleeding post-cannulation due to an incorrect needle puncture. Both grafts were successfully thrombectomized. Primary and secondary patency rates at six months were 60% and 78%, respectively. These patency rates were comparable to those reported for other polyether-urethane and ePTFE grafts. Median time to first cannulation was seven days (3-21) and all puncture sites sealed in less than five minutes.

Impact of graft loss among kidney diseases with a high risk of post-transplant recurrence in the paediatric population

Some kidney diseases tend to recur in the renal allograft after transplantation. We studied the risk of graft loss among primary renal diseases known for their high risk of recurrence and compared it with that of patients with hypoplasia and/or dysplasia. Within the European Society of Paediatric Nephrology and European Renal Association and European Dialysis and Transplant Association (ESPN/ERA-EDTA) registry, we studied children from 33 countries who received a kidney transplant before the age of 20 between 1990 and 2009. Patients were censored after 5 years of follow-up and cumulative incidence competing risk analysis was used to calculate survival curves. Patients with focal and segmental glomerulosclerosis (FSGS), haemolytic uraemic syndrome (HUS), membranoproliferative glomerulonephritis Type I or II (MPGN), IgA nephropathy or Henoch Schönlein Purpura (HSP/IgA) or systemic lupus erythomatosus (SLE) underwent pre-emptive transplantation significantly less often than patients with hypoplasia and/or dysplasia. The rate of living donation was lower among patients with FSGS and SLE than in patients with hypoplasia and/or dysplasia. In comparison with hypoplasia and/or dysplasia patients with a risk of 14.4%, the 5-year risk of graft loss was significantly increased in patients with FSGS (25.7%) and MPGN (32.4%) while it was not significantly increased in children with HUS (18.9%), HSP/IgA (16.3%) or SLE (20.3%). One-year graft survival strongly improved among HUS patients from 17.1% in 1995-1999 to 3.6% in 2005-2009 and was not accompanied by a decrease in the number of transplantations. The risk of graft loss is increased among specific causes of renal failure with a high risk of post-transplant recurrence. It seems likely that, due to anticipation of such risk, physicians perform less pre-emptive transplantation and provide fewer grafts from living related donors in patients with these conditions. Improved risk stratification by physicians, resulting in the identification of patients with HUS at higher or lower risk of recurrence, might explain the much improved graft survival rates.

Arteriovenous fistula aneurysms in patients with Alport's

Alport's syndrome is a rare but important cause of renal failure. It is characterized by Type IV collagen mutations resulting in connective tissue disorders and renal and cochlear dysfunction. Vascular basement membrane also contains collagen IV and the effect on arteriovenous fistulas (AVFs) is not reported. Anecdotally, we observed a high rate of aneurysm formation in Arteriovenous fistulas (AVF) of patients with Alport's and sought to determine whether this was the case within our population. All patients with a diagnosis of Alport's were identified from a contemporaneously maintained database. AVFs formed in patients with Alport's were identified to define the incidence of aneurysms in this group. A total of 40 patients with a diagnosis of Alport's were identified. Of these, 20 patients had undergone AVF formation, the remainder opting for CAPD as renal replacement or had undergone pre-emptive transplantation. Of the 20 patients identified, 11 had an AVF and of these the rate of aneurysm formation was high (55%). While this finding of high rate of aneurysmal AVF in Alport's patients is a purely observational finding within our population further population study would be extremely interesting and could support enhanced surveillance or alternative dialysis modalities in Alport's syndrome patients.

Acute Renal Failure in Diabetes Mellitus (Prospective Study)

Objective: To study the pattern and outcome of acute renal failure (ARF) in diabetes mellitus. Methods: Outcome of variables like duration of renal failure, recovery of renal function and mortality were analyzed with parameters like age, sex, duration of diabetes mellitus, preexisting diabetic nephropathy, preexisting ischemic heart disease, cause of renal failure, dialysis requirement and number of organ systems involved. Results: 70 patients with diabetes mellitus and acute renal failure were studied. Most common causes of acute renal failure were found to be sepsis and urinary tract obstruction. Most common cause of urinary tract obstruction was papillary necrosis. NSAID was most common cause of drug induced renal failure. Out of total 17 patients who underwent renal biopsy, 9 received steroid treatments had AIN, 1 had diffuse proliferative glomerulonephritis (DPGN). Out of 9 patients who had received steroid treatment, 6 patients had recovery of renal failure. Recovery of acute renal failure was found in 64.3% of the study group. Patients with urinary tract obstruction seemed to have better outcome of ARF recovery, when compared with other causes of acute renal failure, though it did not reach statistical significance. Duration of renal failure >10 days seemed to have poor outcome of ARF recovery, though it did not reach statistical significance. Surprisingly patients with sepsis appeared to have better outcome of ARF recovery, compared to other causes of renal failure with statistical significance. Conclusions: Most common causes of renal failure in our study were found to be sepsis and urinary tract obstruction. Acute renal failure recovered in 64.3%. Patients with urinary tract obstruction and sepsis seemed to have favorable outcome in ARF recovery.

Acute kidney injury in patients infected by H1N1 - clinical histological correlation in a series of cases

Influenza A (H1N1) virus was first reported on April 2009 and, since then, several studies have reported the characteristics concerning the clinical presentation and pulmonary involvement. However, accurate information about the acute kidney injury (AKI) and kidney histopathological findings in these patients remain scarce. To describe the kidney histopathological findings of 6 patients with H1N1 who developed AKI and underwent kidney biopsy, correlating them with clinical features. We studied six patients admitted to Hospital de Clínicas UFPR with a PCR-confirmed diagnosis of H1N1who developed ARF and underwent kidney biopsy. We reviewed their medical file and the microscopy findings of the biopsy. Clinical and/or laboratory evidence of AKI was present in all cases, and only one did not present oliguria. Kidney tissues revealed glomerular lesions in two patients: one patient, with systemic lupus erythematosus, showed changes consistent with lupus nephritis class III A-C according to the ISN/RPS 2003 and focal thrombotic microangiopathy; the other one had intercapillary nodular glomerulosclerosis, but without clinical or laboratory evidence of diabetes. Vacuolar degenerative tubular changes were present in all cases, with focus of oxalosis in two cases. Mild to moderate atherosclerosis was found in two patients. In this study, varying degrees of vacuolar degenerative tubular changes were present in all patients, but there were no signs of acute tubular necrosis. It seems that in the present study a prerenal cause of acute renal failure was the main involved mechanim to explain the cause of renal failure in these patients.

Hyperglycemia Decreases the Expression of ATP Synthase &lt;b&gt;&lt;i&gt;β&lt;/i&gt;&lt;/b&gt; Subunit and Enolase 2 in Glomerular Epithelial Cells

Glomerular epithelial cells (GECs) are known to play a key role in maintaining the structure and function of the glomerulus. GEC injury induced by hyperglycemia is present in early-stage diabetic nephropathy (DN), which is the most common cause of renal failure. In an attempt to identify target proteins involved in the pathogenesis of GEC injury at early DN, we performed the proteomic analysis using primary cultures of GECs, prepared from the dissected rat glomeruli. The protein expression profiles in the two-dimensional electrophoresis gels were compared between GECs treated for three days with normal glucose (5 mM) and those with high glucose (30 mM) concentrations. These concentrations correspond to blood glucose concentrations under normoglycemia and hyperglycemia, respectively. Proteins with differential expression levels were identified using ESI-Q-TOF tandem mass spectrometry. The primary GECs cultured in hyperglycemic conditions showed cellular hypertrophy and increased production of reactive oxygen species, both of which reflect the GEC injury. Our proteomic analysis identified eight proteins with differential expression profiles, depending on glucose concentrations. Among them, we selected ATP synthase β subunit and enolase 2 that are related to energy metabolism and are down-regulated under hyperglycemia, and confirmed that hyperglycemia decreased the expression levels of ATP synthase β subunit and enolase 2 proteins by western blotting analysis. Hyperglycemia may impair mitochondrial function and alter glycolysis in GECs by down-regulating the expression of ATP synthase β subunit and enolase 2. The present study may provide a better understanding of the pathogenic mechanisms of GEC injury in early DN.

Irreversible Hemorrhagic Complication of Recurrent Posterior Reversible Encephalopathy Syndrome in a Patient with Systemic Lupus Erythematosus

A diagnosis of posterior reversible encephalopathy syndrome (PRES) is based on a combination of clinical symptoms including headache, altered alertness, abnormalities of visual perception, and seizure, and characteristic neuroimaging findings of transient white matter edema, mostly in the posterior parietal-temporaloccipital regions of the brain (1, 2). Conditions commonly associated with PRES include severe hypertension, eclampsia/ preeclampsia, immunosuppressive medications including cyclosporine and taclorimus, antineoplastic agents, and various cause of renal failure (3, 4). PRES as a complication of systemic lupus erythematosus (PRES-SLE) is not uncommon and neurologic or psychiatric abnormalities occur in up to two-thirds of patients with SLE (4). Usually PRES is reversible vasogenic edema in the posterior circuation territories, although atypical findings such as conversion to irreversible cytotoxic edema, hemorrhage, and enhancement have been described (3). And cytotoxic edema surrounded by extensive vasogenic edema resulted in poor outcome. We report a case of PRESSLE showing irreversible hemorrhagic transformation as a complication of recurrent PRES.

Serum Creatinine Levels Unrelated to Child-Pugh Status in Uncomplicated Cirrhosis of Liver with Ascites

Introduction: Liver cirrhosis and renal failure are two diseases that may occur in conjunction due to mutually related pathological processes. Liver cirrhosis causes portal hypertension that ultimately causes splanchnic vasodilatation leading to hepatorenal syndrome. Hypovolemia is another cause of renal failure in liver cirrhosis. The study presented here was done to assess the renal functions in patients with liver cirrhosis with ascites. Materials and methods: Sixty patients with uncomplicated cirrhosis of liver with ascites with normal renal function were included in this study. All patients were examined physically and biochemical. Main biochemical variables were serum bilirubin, serum albumin, serum creatinine and prothrombin time. Enrolled patients were categorized according to Child-Pugh class B and C. Serum creatinine levels were measured in all cases. Results: Mean level of serum albumin, serum creatinine and prothrombin time among Child B and C classes of liver cirrhosis patients were 27.36 vs 26.84 gm/dl, 0.79 vs 0.93 mg/dl, 15.97 vs 19.26 seconds respectively. No statistically significant change in the serum creatinine level among Child B and C were noticed. Conclusion: This study showed that the effect of liver cirrhosis on renal dysfunction would be minimal, if any.