Urolithiasis, Kidney Transplantation, and Pregnancy and Kidney Disease

2012 ◽  
Author(s):  
Stephen B. Erickson ◽  
Hatem Amer ◽  
Timothy S. Larson
Keyword(s):  
Kidney Stones ◽  
End Stage Renal Disease ◽  
Stone Formation ◽  
Renal Tubules ◽  
Anatomical Changes ◽  
Renal Enlargement ◽  
Ureteral Peristalsis ◽  
Total Body ◽  
Stage Renal Disease ◽  
End Stage

It was previously assumed that all kidney stones crystallized as urine passed through the renal tubules and were retained by means of crystal-tubular cell interactions. Recently uroscopy with papillary biopsies has shown 2 different pathways for stone formation, both mediated by calcium phosphate crystals. Kidney transplant has become the preferred treatment for patients with end-stage renal disease. Those benefiting from transplant included patients who would be deemed "high risk," such as those with diabetes mellitus and those older than 70 years. Anatomical changes associated with pregnancy are renal enlargement and dilatation of the calyces, renal pelvis, and ureters. Physiologic changes include a 30% to 50% increase in glomerular filtration rate and renal blood flow; a mean decrease of 0.5 mg/dL in the creatinine level and a mean decrease of 18 mg/dL in the serum urea nitrogen level; intermittent glycosuria independent of plasma glucose; proteinuria; aminoaciduria; increased uric acid excretion; increased total body water, with osmostat resetting; 50% increase in plasma volume and cardiac output; and increased ureteral peristalsis.

scholarly journals Identifying risk factors for development of nephrolithiasis in end-stage renal disease patients

2019 ◽  
Vol 14 (5) ◽  
Author(s):  
Charles Hesswani ◽  
Sameena Iqbal ◽  
Khashayar Rafat Zand ◽  
Simon Sun ◽  
Bernard Unikowsky ◽  
...  
Keyword(s):  
End Stage Renal Disease ◽  
De Novo ◽  
Stone Formation ◽  
Ionized Calcium ◽  
Lower Serum ◽  
Stone Formers ◽  
Serum Ionized Calcium ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

Introduction: We sought to assess the incidence and risk factors for stone development in patients with end-stage renal disease (ESRD) on hemodialysis (HD). Methods: Medical records of patients receiving HD between 2007 and 2017 were retrospectively reviewed. Patients who had been on HD for at least three months and had imaging studies (computed tomography [CT] scans or ultrasound [US]) pre- and post-initiation of HD were included. Exclusion criterion was presence of stones pre-HD. De novo stones were defined as renal stones found on followup imaging. Demographics, laboratory data, comorbidities, and dialysis characteristics were compared between non-stone-formers and stone-formers using propensity score matching. Results: A total of 133 patients met the inclusion criteria. Their median age was 68.5 years, median body mass index 28.7 kg/m2, and median dialysis duration 59.5 months. After HD, 14 (10.5%) patients developed de novo stones and their median dialysis-to-stone duration was 23.5 months. When compared with non-stone-formers, stone-formers had significantly lower incidence of hypertension (48.2% vs. 14.3%; p=0.03), lower serum ionized calcium (1.16 vs. 1.07 mmol/L; p=0.01) and magnesium (0.95 vs. 0.81 mmol/L; p=0.01), and significantly higher serum uric acid (281.5 vs. 319.0 mmol/L; p=0.03). Multivariate analysis demonstrated that lower serum ionized calcium (adjusted odds ratio [OR] 0.00001; 95% confidence interval [CI] 0–0.18) and magnesium (adjusted OR 0.0003; 95% CI 0–0.59) were significantly associated with stone formation. Conclusions: The incidence of de novo nephrolithiasis in ESRD patients on HD was 10.5%. Increased serum uric acid, decreased serum magnesium and ionized calcium, and absence of hypertension were associated with increased stone-formation in ESRD patients on HD.

scholarly journals Magnesium in Chronic Kidney Disease: Should We Care?

2018 ◽  
Vol 45 (1-3) ◽  
pp. 173-178 ◽  
Author(s):  
Esther R. van de Wal-Visscher ◽  
Jeroen P. Kooman ◽  
Frank M. van der Sande
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
The Body ◽  
Cardiac Conduction ◽  
Increased Risk ◽  
Total Body ◽  
Stage Renal Disease ◽  
End Stage

Background: Magnesium (Mg) is an essential cation for multiple processes in the body. The kidney plays a major role in regulating the Mg balance. In a healthy individual, total-body Mg content is kept constant by interactions among intestine, bones and the kidneys. Summary: In case of chronic kidney disease (CKD), renal regulatory mechanisms may be insufficient to balance intestinal Mg absorption. Usually Mg remains normal; however, when glomerular filtration rate declines, changes in serum Mg are observed. Patients with end-stage renal disease on dialysis are largely dependent on the dialysate Mg concentration for maintaining serum Mg and Mg homeostasis. A low Mg is associated with several complications such as hypertension, and vascular calcification, and also associated with an increased risk for both cardiovascular disease (CVD) and non-CVD mortality. Severe hypermagnesaemia is known to cause cardiac conduction defects, neuromuscular effects and muscle weakness; a slightly elevated Mg has been suggested to be beneficial in patients with end-stage renal disease. Key Messages: The role of both low and high Mg, in general, but especially in relation to CKD and dialysis patients is discussed.

scholarly journals The effect of fluid overload on sleep apnoea severity in haemodialysis patients

2017 ◽  
Vol 49 (4) ◽  
pp. 1601789 ◽  
Author(s):  
Owen D. Lyons ◽  
Toru Inami ◽  
Elisa Perger ◽  
Azadeh Yadollahi ◽  
Christopher T. Chan ◽  
...  
Keyword(s):  
Heart Failure ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Fluid Overload ◽  
Extracellular Fluid ◽  
Sleep Apnoea ◽  
Fluid Volume ◽  
Total Body ◽  
Stage Renal Disease ◽  
End Stage

As in heart failure, obstructive and central sleep apnoea (OSA and CSA, respectively) are common in end-stage renal disease. Fluid overload characterises end-stage renal disease and heart failure, and in heart failure plays a role in the pathogenesis of OSA and CSA. We postulated that in end-stage renal disease patients, those with sleep apnoea would have greater fluid volume overload than those without.End-stage renal disease patients on thrice-weekly haemodialysis underwent overnight polysomnography on a nondialysis day to determine their apnoea–hypopnoea index (AHI). Extracellular fluid volume of the total body, neck, thorax and right leg were measured using bioelectrical impedance.28 patients had an AHI ≥15 (sleep apnoea group; OSA:CSA 21:7) and 12 had an AHI <15 (no sleep apnoea group). Total body extracellular fluid volume was 2.6 L greater in the sleep apnoea group than in the no sleep apnoea group (p=0.006). Neck, thorax, and leg fluid volumes were also greater in the sleep apnoea than the no sleep apnoea group (p<0.05), despite no difference in body mass index (p=0.165).These findings support a role for fluid overload in the pathogenesis of both OSA and CSA in end-stage renal disease.

Cimetidine Disposition in Patients on Continuous Ambulatory Peritoneal Dialysis

1981 ◽  
Vol 2 (2) ◽  
pp. 73-76 ◽  
Author(s):  
Thomas W. Paton ◽  
M. Arifie Manuel ◽  
Scott E. Walker
Keyword(s):  
Peritoneal Dialysis ◽  
Continuous Ambulatory Peritoneal Dialysis ◽  
End Stage Renal Disease ◽  
Total Body Clearance ◽  
Beta Phase ◽  
Male Patients ◽  
Total Body ◽  
Stage Renal Disease ◽  
End Stage ◽  
Body Clearance

The disposition of cimetidine was studied following a single intrave nous dose of 300 mg over 10 minutes in six male patients with end-stage renal disease on continuous ambulatory peritoneal dialysis (CAPD). The infusion of cimetidine and CAPD were initiated simultaneously. Cimetidine disappearance from plasma was biphasic with beta-phase ti varying from 6.1 to 7.4 hours. The total body clearance varied from 138 to 195 ml/min with a peritoneal clearance ranging from 1.9 to 4.0 ml/min. The total amount of cimetidine removed in the dialysate varied from 3.1 to 8.3 mg (1.2 to 2.7% of the dose administered) over 24 hours. This study demonstrates that very little cimetidine is removed by CAPD. We recommend that, to avoid toxicity, patients on CAPD should be given 200 mg cimetidine every 12 hours.

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