Albuminuria as a predictor of mortality in type II diabetic patients after living-donor liver transplantation.

PURPOSE: Diabetes mellitus (DM) increases the risk of morbidity and mortality after liver resection. Albuminuria is associated with a higher risk for all-cause and cardiovascular mortality. This study evaluated albuminuria as a predictor of the outcome of living donor liver transplantation (LDLT) in patients with pre-existing DM. METHODS: This retrospective study involved 103 type II diabetic patients with end-stage liver disease who received LDLT. Preoperative spot urine albumin: creatinine ratio was used to determine the degree of albuminuria. The primary outcome measure was the impact of urinary albumin excretion on the 3-year mortality rate after LDLT in this diabetic cohort. RESULTS: Hepatitis C virus infection was the main cause of cirrhosis. Albuminuria was detected in 41 patients (39.8%); 15 had macroalbuminuria, while 26 had microalbuminuria. Patients with microalbuminuria were significantly older than those with macroalbuminuria and normal albumin in urine. After 3 years, twenty-four patients (23.3%) died within 3 years after LT. Myocardial infarction was the leading cause of death (25%). Albuminuria was an independent factor affecting 3-year mortality with an odds ratio of 5.17 (95% CI: 1.86-14.35). CONCLUSION: Preoperative albuminuria is an independent factor affecting mortality within 3 years after LDLT in type II diabetic patients. Myocardial infarction was the leading cause of death in 25% of cases, followed by hepatocellular carcinoma recurrence, sepsis, and graft failure.KEY MESSAGESDiabetes mellitus (DM) increases the risk of morbidity and mortality after liver resection.Albuminuria is associated with a higher risk for all-cause and cardiovascular mortality.Preoperative albuminuria is a significant predictor of mortality within 3 years after LDLT in diabetic patients.

Serum sclerostin in acute kidney injury patients.

BACKGROUND: Many of the mineral metabolite abnormalities encountered in chronic kidney disease (CKD) patients were found also associated with acute kidney injury (AKI). In the last decade, sclerostin was found to intimately affect bone mineral metabolism in CKD patients. Nothing is known about sclerostin in AKI. OBJECTIVE: We looked for serum level of sclerostin in AKI patients in comparison to normal control subjects and if there is an impact on metabolic derangement, endothelial function or clinical outcome. CASES AND METHODS: This is a cross sectional case control observational study of 219 AKI cases (group I) beside 219 age matched normal control subjects (group II). All cases of group I were in the intensive care because of sepsis; 86 had acute on CKD (group Ib), while 133 had de novo AKI (group Ia). All studied subjects underwent estimation of serum sclerostin, parathyroid hormone (PTH), 25 hydroxy vitamin D (25 OH vit D), fibroblast growth factor 23 (FGF23), C-reactive protein (CRP), interleukin 6 (IL6), Homeostatic Model Assessment for Insulin Resistance (Homa IR), beside the routine CBC, kidney and liver function tests, serum calcium, and phosphorus, and flow mediated vasodilation of brachial artery (FMD). Follow-up of group I cases was done till they recovered or passed away. RESULTS: Serum sclerostin, PTH, FGF23, phosphorus, CRP, IL6, HOMA IR, creatinine, urea, uric acid, ALT, AST and white blood cell count (WBC) were significantly higher while serum calcium, 25 OH vit D, hemoglobin, platelet count and FMD were significantly lower in group I compared to group II (P<0.001 in all). On the other hand, there was no significant difference in serum sclerostin, PTH, FGfF23, 25 OH vit D, CRP, IL6, Homa IR and FMD between group Ia and Ib. Survivors were younger in age (median 55.5 vs. 60 years, P<0.04), had lower AST (30.5 vs. 58 units, P<0.001), had higher platelet count (206 vs 162×109/L, P<0.001), otherwise, there was no significant difference in any of the other parameters between survivors and patients that were lost. Serum sclerostin had strong correlation with FGF23 in group I (r=0.99, P<0.001) and group II (r=1, P<0.001). Homa IR had positive correlation with serum sclerostin (r=0.148, P=0.014) and serum FGF23 (r=0.142, P=0.018) in group I. CONCLUSION: Sclerostin is intimately related to FGF23. Sclerostin level increases in AKI patients. Both sclerostin and FGF23 might increase insulin resistance but have no impact on FMD. Neither sclerostin nor FGF23 interfere with AKI outcome.

Serum sclerostin in acute kidney injury patients / Esclerostina sérica en pacientes con lesión renal aguda

Background: Many of the mineral metabolite abnormalities encountered in chronic kidney disease (CKD) patients were found also associated with acute kidney injury (AKI). In the last decade, sclerostin was found to intimately affect bone mineral metabolism in CKD patients. Nothing is known about sclerostin in AKI.ObjectiveWe looked for serum level of sclerostin in AKI patients in comparison to normal control subjects and if there is an impact on metabolic derangement, endothelial function or clinical outcome.Cases and methodsThis is a cross sectional case control observational study of 219 AKI cases (group I) beside 219 age matched normal control subjects (group II). All cases of group I were in the intensive care because of sepsis; 86 had acute on CKD (group Ib), while 133 had de novo AKI (group Ia). All studied subjects underwent estimation of serum sclerostin, parathyroid hormone (PTH), 25 hydroxy vitamin D (25 OH vit D), fibroblast growth factor 23 (FGF23), C-reactive protein (CRP), interleukin 6 (IL6), Homeostatic Model Assessment for Insulin Resistance (Homa IR), beside the routine CBC, kidney and liver function tests, serum calcium, and phosphorus, and flow mediated vasodilation of brachial artery (FMD). Follow-up of group I cases was done till they recovered or passed away.ResultsSerum sclerostin, PTH, FGF23, phosphorus, CRP, IL6, HOMA IR, creatinine, urea, uric acid, ALT, AST and white blood cell count (WBC) were significantly higher while serum calcium, 25 OH vit D, hemoglobin, platelet count and FMD were significantly lower in group I compared to group II (P<0.001 in all). On the other hand, there was no significant difference in serum sclerostin, PTH, FGfF23, 25 OH vit D, CRP, IL6, Homa IR and FMD between group Ia and Ib. (AU)

Antecedentes: Muchas de las anomalías de los metabolitos minerales que se encuentran en el riñón de los pacientes con enfermedad renal crónica (ERC) también se asociaron con lesión renal aguda (IRA). En la última década, se ha descubierto que la esclerostina afectaba íntimamente al metabolismo mineral óseo en pacientes con ERC. No se sabe nada sobre la esclerostina en la LRA.ObjetivoBuscamos el nivel sérico de esclerostina en pacientes con IRA en comparación con los niveles normales en sujetos de control, y si hay un impacto en el trastorno metabólico, la función endotelial o el resultado clínico.Casos y métodosEste es un estudio observacional transversal de casos y controles de 219 casos de IRA (grupo I) además de 219 sujetos de control normales de la misma edad (grupo II). Todos los casos del grupo I se hallaban en cuidados intensivos por sepsis; 86 tenían ERC aguda (grupo Ib), mientras que 133 tenía de novo AKI (grupo Ia). Todos los sujetos estudiados se sometieron a una estimación de la esclerostina sérica, hormona paratiroidea (PTH), 25 hidroxi vitamina D (25 OH vit D), factor de crecimiento de fibroblastos 23 (FGF23), proteína C reactiva (CRP), interleucina 6 (IL6), evaluación del modelo homeostático para resistencia a la insulina (Homa IR), además del hemograma completo de rutina, pruebas de función renal y hepática, suero calcio y fósforo, y vasodilatación de la arteria braquial (FMD) mediada por flujo. El seguimiento de los casos del grupo I se realizó hasta que se recuperaron o fallecieron.ResultadosEsclerostina sérica, PTH, FGF23, fósforo, PCR, IL6, HOMA IR, creatinina, urea, ácido úrico, ALT, AST y recuento de glóbulos blancos (WBC) fueron significativamente más altos mientras que el suero calcio, 25 OH vit D, hemoglobina, recuento de plaquetas y fiebre aftosa fueron significativamente más bajos en el grupo I en comparación con el grupo II (p<0,001 en total). (AU)

Serum sclerostin in acute kidney injury patients.

BACKGROUND: Many of the mineral metabolite abnormalities encountered in chronic kidney disease (CKD) patients were found also associated with acute kidney injury (AKI). In the last decade, sclerostin was found to intimately affect bone mineral metabolism in CKD patients. Nothing is known about sclerostin in AKI. OBJECTIVE: We looked for serum level of sclerostin in AKI patients in comparison to normal control subjects and if there is an impact on metabolic derangement, endothelial function or clinical outcome. CASES AND METHODS: This is a cross sectional case control observational study of 219 AKI cases (group I) beside 219 age matched normal control subjects (group II). All cases of group I were in the intensive care because of sepsis; 86 had acute on CKD (group Ib), while 133 had de novo AKI (group Ia). All studied subjects underwent estimation of serum sclerostin, parathyroid hormone (PTH), 25 hydroxy vitamin D (25 OH vit D), fibroblast growth factor 23 (FGF23), C-reactive protein (CRP), interleukin 6 (IL6), Homeostatic Model Assessment for Insulin Resistance (Homa IR), beside the routine CBC, kidney and liver function tests, serum calcium, and phosphorus, and flow mediated vasodilation of brachial artery (FMD). Follow-up of group I cases was done till they recovered or passed away. RESULTS: Serum sclerostin, PTH, FGF23, phosphorus, CRP, IL6, HOMA IR, creatinine, urea, uric acid, ALT, AST and white blood cell count (WBC) were significantly higher while serum calcium, 25 OH vit D, hemoglobin, platelet count and FMD were significantly lower in group I compared to group II (P<0.001 in all). On the other hand, there was no significant difference in serum sclerostin, PTH, FGfF23, 25 OH vit D, CRP, IL6, Homa IR and FMD between group Ia and Ib. Survivors were younger in age (median 55.5 vs. 60 years, P<0.04), had lower AST (30.5 vs. 58 units, P<0.001), had higher platelet count (206 vs 162×109/L, P<0.001), otherwise, there was no significant difference in any of the other parameters between survivors and patients that were lost. Serum sclerostin had strong correlation with FGF23 in group I (r=0.99, P<0.001) and group II (r=1, P<0.001). Homa IR had positive correlation with serum sclerostin (r=0.148, P=0.014) and serum FGF23 (r=0.142, P=0.018) in group I. CONCLUSION: Sclerostin is intimately related to FGF23. Sclerostin level increases in AKI patients. Both sclerostin and FGF23 might increase insulin resistance but have no impact on FMD. Neither sclerostin nor FGF23 interfere with AKI outcome.

Incidence and Characteristics of de novo Renal Cryoglobulinemia After Direct-Acting Antivirals Treatment in an Egyptian Hepatitis C Cohort.

INTRODUCTION: The side effects profile of the new direct--acting antivirals for the treatment of hepatitis C virus (HCV) is not fully elucidated. OBJECTIVE: In this cross-sectional study, we aim to describe the incidence and characteristics of a novel observation of de novo renal cryoglobulinemic glomerulonephritis after successful treatment with DAA. METHODOLOGY: A total of 12,985 Hepatitis C Patients (genotype IV) received the new DAA. After successful treatment, patients with deranged renal functions or proteinuria were referred to the nephrology department for assessment. The clinical manifestations ranged from lower limb edema to the development of purpura skin lesions. Cryoglobulins were tested in the serum using the PCR detection. RESULTS: Fifty patients had detectable de novo cryoglobulins in the serum. The most common type in renal biopsies was membranoproliferative glomerulonephritis (52%) and chronic kidney disease (CKD) developed in 46% of cases. CONCLUSION: De novo cryoglobulinemic glomerulonephritis and progression to CKD may rarely complicate successful treatment of HCV using direct-acting antivirals.