The Role of the Artificial Kidney in Correcting Serum Electrolyte Abnormalities in Renal Failure: Report of Four Representative Cases

Objective: To review disorders elements of the metabolic syndrome in patients with end-stage chronic renal failure on dialysis cycle. Materials and methods: A cross sectional descriptive study of 85 patients including end-stage chronic renal failure in dialysis cycle from 5/2015 - 9/2016 at the Department of Artificial Kidney, Hue Central Hospital. Results: The prevalence of metabolic syndrome in dialysis patients was 37.65%. The prevalence of abdominal obesity was 30.6%; The prevalence of hypertension was 72.9%, the average value systolic blood pressure and diastolic blood pressure were 142.24 ± 27.53, 80.35 ± 12.48 mmHg; The prevalence of hyperglycemia was 28%, the average value blood glucose was 4.9 ± 1.19 mmol/l; The prevalence of triglyceride increase was 34.1%, the average value triglyceride was 1.59 ± 0.84 mmol/l. The prevalence of HDL-C increase was 47.1%, the average value HDL-C was 1.24 ± 0.33 mmol/l. Conclusion: The prevalence of metabolic syndrome in dialysis patients is very high, in which hypertension and HDL disturbances are the highest. Key words: chronic renal failure, dialysis, metabolic syndrome

Download Full-text

Role of uremic toxins in exacerbating anemia in renal failure

Kidney International ◽

10.1046/j.1523-1755.2001.07821.x ◽

2001 ◽

Vol 59 (s78) ◽

pp. 67-72 ◽

Cited By ~ 30

Author(s):

Iain C. Macdougall

Keyword(s):

Renal Failure ◽

Uremic Toxins

Download Full-text

Interleukin-6 Could Be a Potential Prognostic Factor in Ambulatory Elderly Patients with Stable Heart Failure: Results from a Pilot Study

Journal of Clinical Medicine ◽

10.3390/jcm10030504 ◽

2021 ◽

Vol 10 (3) ◽

pp. 504

Author(s):

Marina Povar-Echeverría ◽

Pablo Esteban Auquilla-Clavijo ◽

Emmanuel Andrès ◽

Francisco Javier Martin-Sánchez ◽

María Victoria Laguna-Calle ◽

...

Keyword(s):

Heart Failure ◽

Atrial Fibrillation ◽

Renal Failure ◽

Interleukin 6 ◽

Kaplan Meier ◽

Patients With Heart Failure ◽

Potential Prognostic Factor ◽

Fundamental Phenomenon ◽

Group 2

Introduction: Inflammation is a fundamental phenomenon in heart failure, but the prognostic or therapeutic role of markers such as interleukin-6 (IL-6) has not yet been clarified. The objective of this study is to describe the clinical profile of patients with elevated IL-6 and determine if they have worse clinical outcomes. Methods: A retrospective c.ohort observational study including 78 patients with heart failure followed up at the Heart Failure Outpatient Clinic of the Internal Medicine Department. IL-6 was determined in all patients, who were then assigned into two groups according to IL-6 level (normal or high). Clinical and prognostic data were collected to determine the differences in both groups. Results: The average age was 79 years, 60% female. A total of 53.8% of the patients had elevated IL-6 (group 2). Patients with elevated IL-6 presented more frequently with anemia mellitus (64.3% vs. 41.7%; p = 0.046), atrial fibrillation (83.3% vs. 61.9% p = 0.036), dyslipidemia (76.2% vs. 58.2%; p = 0.03), higher creatinine levels (1.35 mg/dL vs. 1.08 mg/dL; p = 0.024), lower glomerular filtration rate (43.6 mL/min/m2 vs. 59.9 mL/min/m2; p = 0.007), and anemia 25% vs. 52.4% p = 0.014. The factors independently associated with the increase in IL-6 were anemia 3.513 (1.163–10.607) and renal failure 0.963 (0.936–0.991), p < 0.05. Mortality was higher in the group with elevated IL-6 levels (16% vs. 2%; p = 0.044) with a log-rank p = 0.027 in the Kaplan–Meier curve. Conclusion: Patients with heart failure and elevated IL-6 most often have atrial fibrillation, diabetes mellitus, dyslipidemia, anemia, and renal failure. In addition, mortality was higher and a tendency of higher hospital admission was observed in stable HF patients with elevated IL-6.

Download Full-text

Novel Variant in CLDN16: A Further Step in the Diagnosis of Familial Hypomagnesemia with Hypercalciuria and Nephrocalcinosis—A Case Report

Uro ◽

10.3390/uro1030011 ◽

2021 ◽

Vol 1 (3) ◽

pp. 76-81

Author(s):

Gopal Narang ◽

Tim Shimon ◽

Jonathan Moore ◽

Megan Hager ◽

Filippo Pinto e Vairo ◽

...

Keyword(s):

Renal Failure ◽

Clinical Manifestations ◽

Tight Junction Proteins ◽

Early Progression ◽

Significant Burden ◽

Novel Variant ◽

Familial Hypomagnesemia ◽

Calcium And Magnesium ◽

Junction Proteins ◽

Electrolyte Abnormalities

Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is a rare tubulopathy characterized by renal loss of calcium and magnesium leading to progressive renal failure. The disorder is caused by variants to the tight junction proteins claudin-16 and -19. While rare, this disorder causes a significant burden to patients based on its clinical manifestations of various electrolyte abnormalities, nephrocalcinosis, and early progression to renal failure. In this report we describe the diagnosis of a novel variant of CLDN16 which clinically presented with severe hypomagnesemia, hypocalcemia, nephrocalcinosis, and renal failure.

Download Full-text

Role of parathyroid hormone in the glucose intolerance of chronic renal failure.

Journal of Clinical Investigation ◽

10.1172/jci111765 ◽

1985 ◽

Vol 75 (3) ◽

pp. 1037-1044 ◽

Cited By ~ 99

Author(s):

M Akmal ◽

S G Massry ◽

D A Goldstein ◽

P Fanti ◽

A Weisz ◽

...

Keyword(s):

Renal Failure ◽

Parathyroid Hormone ◽

Chronic Renal Failure ◽

Glucose Intolerance

Download Full-text

HUS and the case for complement

Blood ◽

10.1182/blood-2015-03-569277 ◽

2015 ◽

Vol 126 (18) ◽

pp. 2085-2090 ◽

Cited By ~ 17

Author(s):

Edward M. Conway

Keyword(s):

Escherichia Coli ◽

Renal Failure ◽

Shiga Toxin ◽

Complement Activation ◽

Thrombotic Microangiopathy ◽

Response To Treatment ◽

Microangiopathic Hemolytic Anemia ◽

New Knowledge ◽

Uremic Syndrome

Abstract Hemolytic-uremic syndrome (HUS) is a thrombotic microangiopathy that is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and renal failure. Excess complement activation underlies atypical HUS and is evident in Shiga toxin–induced HUS (STEC-HUS). This Spotlight focuses on new knowledge of the role of Escherichia coli–derived toxins and polyphosphate in modulating complement and coagulation, and how they affect disease progression and response to treatment. Such new insights may impact on current and future choices of therapies for STEC-HUS.

Download Full-text

Disruption of renal peritubular blood flow in lipopolysaccharide-induced renal failure: role of nitric oxide and caspases

AJP Renal Physiology ◽

10.1152/ajprenal.00124.2005 ◽

2005 ◽

Vol 289 (6) ◽

pp. F1324-F1332 ◽

Cited By ~ 82

Author(s):

Manish M. Tiwari ◽

Robert W. Brock ◽

Judit K. Megyesi ◽

Gur P. Kaushal ◽

Philip R. Mayeux

Keyword(s):

Nitric Oxide ◽

Renal Failure ◽

Blood Flow ◽

Saline Group ◽

No Production ◽

Capillary Perfusion ◽

Peritubular Capillary ◽

Synthase Inhibitor ◽

Peritubular Capillary Perfusion

Acute renal failure (ARF) is a frequent and serious complication of endotoxemia caused by lipopolysaccharide (LPS) and contributes significantly to mortality. The present studies were undertaken to examine the roles of nitric oxide (NO) and caspase activation on renal peritubular blood flow and apoptosis in a murine model of LPS-induced ARF. Male C57BL/6 mice treated with LPS ( Escherichia coli) at a dose of 10 mg/kg developed ARF at 18 h. Renal failure was associated with a significant decrease in peritubular capillary perfusion. Vessels with no flow increased from 7 ± 3% in the saline group to 30 ± 4% in the LPS group ( P < 0.01). Both the inducible NO synthase inhibitor l- N6-1-iminoethyl-lysine (l-NIL) and the nonselective caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp fluoromethylketone (Z-VAD) prevented renal failure and reversed perfusion deficits. Renal failure was also associated with an increase in renal caspase-3 activity and an increase in renal apoptosis. Both l-NIL and Z-VAD prevented these changes. LPS caused an increase in NO production that was blocked by l-NIL but not by Z-VAD. Taken together, these data suggest NO-mediated activation of renal caspases and the resulting disruption in peritubular blood flow are an important mechanism of LPS-induced ARF.

Download Full-text