Depressive symptoms may be associated with fluid and dietary non-adherence which could lead to poorer outcomes. The purpose of this study was to examine the relationship between depressive symptoms and fluid and dietary adherence in 100 patients with end-stage renal disease (ESRD) receiving haemodialysis. A descriptive, cross-sectional design with a convenience sample of 100 patients with ESRD receiving maintenance haemodialysis completed instruments that measured self reported depressive symptoms and perceived fluid and dietary adherence. Demographic and clinical data and objective indicators of fluid and diet adherence were extracted from medical records. As many as two thirds of these subjects exhibited depressive symptoms and half were non-adherent to fluid and diet prescriptions. After controlling for known covariates, patients determined to have moderate to severe depressive symptoms were more likely to report nonadherence to fluid and diet restrictions. Depressive symptoms in patients with ESRD are common and may contribute to dietary and fluid non-adherence. Early identification and appropriate interventions may potentially lead to improvement in adherence of these patients.

These data suggest the possibility of beneficial effects of isoflavone-rich soy foods on the inflammatory and nutritional status of HD patients with underlying systemic inflammation.

There is no correlation between iPTH and bone turnover in African Americans with ESRD. A substantial number of African American patients with low bone turnover have very high serum PTH levels. Bone histomorphometric results reveal differences in remodeling dynamics and responses to PTH between African American and Caucasian patients. Further studies utilizing newer PTH measurement assays are needed to better delineate the correlation between PTH and bone turnover in the various racial groups.

In anesthetized rats we tested the hypothesis that amphotericin B (AmB) reduces glomerular filtration rate (GFR) by activating the tubuloglomerular feedback (TGF) mechanism. Infusion of 1 mg/kg AmB over 50 min was followed by a reduction in kidney GFR (from 0.47±0.03 to 039±0.02 ml/min per 100 g body wt during the second hour after infusion; P < 0.05) and by an increase in urine flow and urinary chloride excretion. Singlenephron GFR (SNGFR) measured in proximal (TGF interrupted) or distal tubules (TGF intact) decreased to a similar degree from 33.4±1.8 and 30.6±1.2 nl/min in the control period to 19.7±1.9 and 21.2±1.6 nl/min during the second hour after AmB infusion (P < 0.05). Distal chloride concentrations and TGF responses to changes in loop of Henle flow rate were not significantly altered by AmB. AmB at 10' M reduced the diameter of isolated perfused afferent arterioles from rabbit kidneys. In isometrically contracting rings of rabbit aorta and renal artery in vitro AmB produced endothelium-independent constriction, with half-maximal contraction (ECu,) being achieved by 1.8 X 10' and 2.6 X 10' M in intact vessels and 1.3 X 10-' and 1.7 X 10' M in endothelium-denuded vessels respectively. Tension development did not occur in Ca-free media or in the presence of Ca channel blockers. Pretreatment with ouabain or Bay K 8644 potentiated the effect of AmB. The vasoconstrictive effect of AmB was counteracted by aminophylline and atrial natriuretic peptide. We conclude that the AmBinduced reduction in GFR is not caused by TGF activation and that AmB has a direct vasoconstrictor effect that is probably initiated by depolarization-induced opening of Ca channels. This effect may be an important component of the nephrotoxic actions of AmB. (J. Clin.

No abstract

The number of nonrenal solid-organ transplants increased substantially in the last few decades. Many of these patients develop renal failure and receive kidney transplantation. The aim of this study was to evaluate patient and kidney allograft survival in primary, repeat, and kidney-after-nonrenal organ transplantation using national data reported to United Network for Organ Sharing (UNOS) from January 2000 through December 2014. Survival time for each patient was stratified into the following: Group A (comparison group)-recipients of primary kidney transplant (178 947 patients), Group B-recipients of repeat kidney transplant (17 819 patients), and Group C-recipients of kidney transplant performed after either a liver, heart, or lung transplant (2365 patients). We compared survivals using log-rank test. Compared to primary or repeat kidney transplant, patient and renal allograft survival was significantly lower in those with previous nonrenal organ transplant. Renal allograft and patient survival after liver, heart, or lung transplants are comparable. Death was the main cause of graft loss in patients who had prior nonrenal organ transplant.

Background: In dialysis and renal transplant patients with secondary and tertiary hyperparathyroidism (HPT), the value of intraoperative parathyroid hormone (ioPTH) during parathyroidectomy (PTX) and its association with long-term PTH levels are unknown. The present study aims at evaluating the relationship of ioPTH with long-term PTH levels post-PTX in dialysis and renal transplant patients in a single-center study. Methods: The ioPTH was measured in 57 dialysis patients (33 females and 24 males) and 18 renal transplant recipients (12 males and 6 females) who underwent PTX from 2005 to 2015 for refractory HPT. Near-total PTX was performed in 56 patients and total PTX with autotransplantation in 20 patients. The PTH monitoring included 3 samples: pre-intubation, 10- and 20-min (pre-ioPTH, 10-ioPTH, and 20-ioPTH) post parathyroid gland excision. Patients were followed up for up to 5 years. Results: In the dialysis group, the median (25th–75th percentile) pre-, 10-, and 20-ioPTH levels were 1,447 pg/mL (938–2,176), 143 pg/mL (78–244) and 112 pg/mL (59–153) respectively. In the renal transplant group, pre-, 10-, and 20-ioPTH levels were 273 pg/mL (180–403), 42 pg/mL (25–72), and 34 pg/mL (23–45) respectively. All patients in the transplant group had a functional kidney transplant at the time of PTX with a median serum creatinine of 1.3 mg/dL (1.2–1.7) and estimated glomerular filtration rate of 55 mL/min (40–60). The median time between renal transplant and PTX surgeries was 22 months (7–81). The last median follow-up PTH level was 66 pg/mL (15–201) in the dialysis group and 54 pg/mL (17–72) in the transplant group (p = 0.438). The mean time for last PTH post-PTX was 2.3 ± 2.0 years. In both groups, there was no significant difference between 20-ioPTH and any-time post-PTX PTH levels (p = 0.6 and p = 0.9). Nineteen patients (25%) were readmitted within 90 days because of hypocalcemia. One patient in the dialysis group was readmitted for post-PTX hematoma evacuation. No patient required repeat PTX because of recurrent HPT that was refractory to medical therapy. Only one dialysis patient required repeat PTX because the first procedure failed. Conclusions: The 20-ioPTH is a good indicator of long-term PTH levels in dialysis and renal transplant patients. Hypocalcemia is a common complication, particularly in dialysis patients, and it is the main reason for readmission after PTX. Hypoparathyroidism is a potential concern after PTX in dialysis patients.

Studies suggest a J-shaped association between blood pressure and cardiovascular events in the setting of intensive systolic blood pressure control; whether there is a similar association with stroke remains less well established. The Secondary Prevention of Small Subcortical Strokes was a randomized trial to evaluate higher (130-149 mmHg) vs. lower (<130 mmHg) systolic blood pressure targets (ClinicalTrials.gov NCT 00059306) in participants with recent lacunar infarcts. We evaluated the association of mean achieved blood pressure, 6 months after randomization, and recurrent stroke, major vascular events, and all-cause mortality. After a mean follow up of 3.7 years, there was a J-shaped association between achieved blood pressure and outcomes; the lowest risk was at approximately124 and 67 mmHg systolic and diastolic, respectively. For example, above a systolic blood pressure of 124 mmHg, one standard deviation higher (11.1 mmHg) was associated with increased mortality (adjusted hazard ratio: 1.9; 95% confidence interval: 1.4, 2.7), whereas below this level, this relationship was inverted (0.29; 0.10, 0.79), p<0.001 for interaction. Above a diastolic blood pressure of 67 mmHg, a one standard deviation higher (8.2 mmHg) was associated with an increased risk of stroke (2.2; 1.4, 3.6), whereas below this level, the association was in the opposite direction (0.34; 0.13, 0.89), p=0.02 for interaction. The lowest risk of all events occurred at a nadir of approximately 120-128 mmHg systolic and 65-70 mmHg diastolic. Future studies should evaluate the impact of excessive blood pressure reduction, especially in older populations with pre-existing vascular disease.