A Successful Approach to Kidney Transplantation in Patients With Enteric (Secondary) Hyperoxaluria

Background. Enteric hyperoxaluria due to malabsorption may cause chronic oxalate nephropathy and lead to end-stage renal disease. Kidney transplantation is challenging given the risk of recurrent calcium-oxalate deposition and nephrolithiasis. Methods. We established a protocol to reduce plasma oxalic acid levels peritransplantation based on reduced intake and increased removal of oxalate. The outcomes of 10 kidney transplantation patients using this protocol are reported. Results. Five patients received a living donor kidney and had immediate graft function. Five received a deceased donor kidney and had immediate (n = 1) or delayed graft function (n = 4). In patients with delayed graft function, the protocol was prolonged after transplantation. In 3 patients, our protocol was reinstituted because of late complications affecting graft function. One patient with high-output stoma and relatively low oxalate levels had lost her first kidney transplant because of recurrent oxalate depositions but now receives intravenous fluid at home on a routine basis 3 times per week to prevent dehydration. Patients are currently between 3 and 32 months after transplantation and all have a stable estimated glomerular filtration rate (mean, 51 +/- 21 mL/min per 1.73 m(2)). In 4 of 8 patients who underwent for cause biopsies after transplantation oxalate depositions were found. Conclusions. This is the first systematic description of kidney transplantation in a cohort of patients with enteric hyperoxaluria. Common complications after kidney transplantation impact long-term transplant function in these patients. With our protocol, kidney transplantation outcomes were favorable in this population with unfavorable transplantation prospects and even previous unsuccessful transplants

Risk factors for muscle loss in hemodialysis patients with high comorbidity

With expanding kidney transplantation programs, remaining hemodialysis patients are more likely to have a high comorbidity burden and may therefore be more prone to lose muscle mass. Our aim was to analyze risk factors for muscle loss in hemodialysis patients with high comorbidity. Fifty-four chronic hemodialysis patients (Charlson Comorbidity Index 9.0 ± 3.4) were followed for 20 weeks using 4-weekly measurements of lean tissue mass, intracellular water, and body cell mass (proxies for muscle mass), handgrip strength (HGS), and biochemical parameters. Mixed models were used to analyze covariate effects on LTM. LTM (−6.4 kg, interquartile range [IQR] −8.1 to −4.8), HGS (−1.9 kg, IQR −3.1 to −0.7), intracellular water (−2.11 L, IQR −2.9 to −1.4) and body cell mass (−4.30 kg, IQR −5.9 to −2.9) decreased in all patients. Conversely, adipose tissue mass increased (4.5 kg, IQR 2.7 to 6.2), resulting in no significant change in body weight (−0.5 kg, IQR −1.0 to 0.1). Independent risk factors for LTM loss over time were male sex (−0.26 kg/week, 95% CI −0.33 to −0.19), C-reactive protein above median (−0.1 kg/week, 95% CI −0.2 to −0.001), and baseline lean tissue index ≥10th percentile (−1.6 kg/week, 95% CI −2.1 to −1.0). Age, dialysis vintage, serum albumin, comorbidity index, and diabetes did not significantly affect LTM loss over time. In this cohort with high comorbidity, we found universal and prominent muscle loss, which was further accelerated by male sex and inflammation. Stable body weight may mask muscle loss because of concurrent fat gain. Our data emphasize the need to assess body composition in all hemodialysis patients and call for studies to analyze whether intervention with nutrition or exercise may curtail muscle loss in the most vulnerable hemodialysis patients

A Successful Approach to Kidney Transplantation in Patients With Enteric (Secondary) Hyperoxaluria

Background. Enteric hyperoxaluria due to malabsorption may cause chronic oxalate nephropathy and lead to end-stage renal disease. Kidney transplantation is challenging given the risk of recurrent calcium-oxalate deposition and nephrolithiasis. Methods. We established a protocol to reduce plasma oxalic acid levels peritransplantation based on reduced intake and increased removal of oxalate. The outcomes of 10 kidney transplantation patients using this protocol are reported. Results. Five patients received a living donor kidney and had immediate graft function. Five received a deceased donor kidney and had immediate (n = 1) or delayed graft function (n = 4). In patients with delayed graft function, the protocol was prolonged after transplantation. In 3 patients, our protocol was reinstituted because of late complications affecting graft function. One patient with high-output stoma and relatively low oxalate levels had lost her first kidney transplant because of recurrent oxalate depositions but now receives intravenous fluid at home on a routine basis 3 times per week to prevent dehydration. Patients are currently between 3 and 32 months after transplantation and all have a stable estimated glomerular filtration rate (mean, 51 ± 21 mL/min per 1.73 m2). In 4 of 8 patients who underwent for cause biopsies after transplantation oxalate depositions were found. Conclusions. This is the first systematic description of kidney transplantation in a cohort of patients with enteric hyperoxaluria. Common complications after kidney transplantation impact long-term transplant function in these patients. With our protocol, kidney transplantation outcomes were favorable in this population with unfavorable transplantation prospects and even previous unsuccessful transplants