BK nephropathy in the native kidneys of patients with organ transplants: Clinical spectrum of BK infection

Nephropathy secondary to BK virus, a member of the Papoviridae family of viruses, has been recognized for some time as an important cause of allograft dysfunction in renal transplant recipients. In recent times, BK nephropathy(BKN) of the native kidneys has being increasingly recognized as a cause of chronic kidney disease in patients with solid organ transplants, bone marrow transplants and in patients with other clinical entities associated with immunosuppression. In such patients renal dysfunction is often attributed to other factors including nephrotoxicity of medications used to prevent rejection of the transplanted organs. Renal biopsy is required for the diagnosis of BKN. Quantitation of the BK viral load in blood and urine are surrogate diagnostic methods. The treatment of BKN is based on reduction of the immunosuppressive medications. Several compounds have shown antiviral activity, but have not consistently shown to have beneficial effects in BKN. In addition to BKN, BK viral infection can cause severe urinary bladder cystitis, ureteritis and urinary tract obstruction as well as manifestations in other organ systems including the central nervous system, the respiratory system, the gastrointestinal system and the hematopoietic system. BK viral infection has also been implicated in tumorigenesis. The spectrum of clinical manifestations from BK infection and infection from other members of the Papoviridae family is widening. Prevention and treatment of BK infection and infections from other Papovaviruses are subjects of intense research.

Nephropathy in dietary hyperoxaluria:A potentially preventable acute or chronic kidney disease

Hyperoxaluria can cause not only nephrolithiasis and nephrocalcinosis,but also renal parenchymal disease histologically characterized by deposition of calcium oxalate crystals throughout the renal parenchyma,profound tubular damage and interstitial inflammation and fibrosis.Hyperoxaluric nephropathy presents clinically as acute or chronic renal failure that may progress to endstage renal disease(ESRD).This sequence of events,well recognized in the past in primary and enteric hyperoxalurias,has also been documented in a few cases of dietary hyperoxaluria.Estimates of oxalate intake in patients with chronic dietary hyperoxaluria who developed chronic kidney disease or ESRD were comparable to the reported average oxalate content of the diets of certain populations worldwide,thus raising the question whether dietary hyperoxaluria is a primary cause of ESRD in these regions.Studies addressing this question have the potential of improving population health and should be undertaken,alongside ongoing studies which are yielding fresh insights into the mechanisms of intestinal absorption and renal excretion of oxalate,and into the mechanisms of development of oxalate-induced renal parenchymal disease.Novel preventive and therapeutic strategies for treating all types of hyperoxaluria are expected to develop from these studies.

Prolonged hypernatremia triggered by hyperglycemic hyperosmolar state with coma: A case report

A man with past lithium use for more than 15 years, but off lithium for two years and not carrying the diagnosis of diabetes mellitus or nephrogenic diabetes insipidus(NDI), presented with coma and hyperglycemic hyperosmolar state(HHS). Following correction of HHS, he developed persistent hypernatremia accompanied by large volumes of urine with low osmolality and no response to desmopressin injections. Urine osmolality remained < 300 m Osm/kg after injection of vasopressin. Improvement in serum sodium concentration followed the intake of large volumes of water plus administration of amiloride and hydrochlorothiazide. Severe hyperglycemia may trigger symptomatic lithium-induced NDI years after cessation of lithium therapy. Patients with newonset diabetes mellitus who had been on prolonged lithium therapy in the past require monitoring of their serum sodium concentration after hyperglycemic episodes regardless of whether they do or do not carry the diagnosis of NDI.

Advanced wasting in peritoneal dialysis patients

AIM To identify patients with end-stage renal disease treated by peritoneal dialysis(PD) who had zero body fat(BF) as determined by analysis of body composition using anthropometric formulas estimating body water(V) and to compare nutritional parameters between these patients and PD patients whose BF was above zero.METHODS Body weight(W) consists of fat-free mass(FFM) andBF.Anthropometric formulas for calculating V allow the calculation of FFM as V/0.73,where 0.73 is the water fraction of FFM at normal hydration.Wasting from loss of BF has adverse survival outcomes in PD.Advanced wasting was defined as zero BF when V/0.73 is equal to or exceeds W.This study,which analyzed 439 PD patients at their first clearance study,used the Watson formulas estimating V to identify patients with V_(Watson)/0.73 ≥ W and compared their nutritional indices with those of PD patients with V_(Watson)/0.73 < W.RESULTS The study identified at the first clearance study two male patients with V_(Watson)/0.73 ≥ W among 439 patients on PD.Compared to 260 other male patients on PD,the two subjects with advanced wasting had exceptionally low body mass index and serum albumin concentration.The first of the two subjects also had very low values for serum creatinine concentration and total(in urine and spent peritoneal dialysate) creatinine excretion rate while the second subject had an elevated serum creatinine concentration and high creatinine excretion rate due,most probably,to non-compliance with the PD prescription.CONCLUSION Advanced wasting(zero BF) in PD patients,identified by the anthropometric formulas that estimate V,while rare,is associated with indices of poor somatic and visceral nutrition.

Reproducibility of serial creatinine excretion measurements in peritoneal dialysis

AIMTo test whether muscle mass evaluated by creatinine excretion （EXCr） is maintained in patients with end-stage kidney disease （ESKD） treated by peritoneal dialysis （PD）, we evaluated repeated measurements of EXCr in a PD population.METHODSOne hundred and sixty-six PD patients （94 male, 72 female） receiving the same PD dose for the duration of the study （up to approximately 2.5 years） had repeated determinations of total （in urine plus spent dialysate） 24-h EXCr （EXCr T） to assess the adequacy of PD by creatinine clearance. All 166 patients had two EXCr T determinations, 84 of the 166 patients had three EXCr T determinations and 44 of the 166 patients had four EXCr T measurements. EXCr T values were compared using the paired t test in the patients who had two studies and by repeated measures ANOVA in those who were studied three or four times.RESULTSIn patients who were studied twice, with the first and second EXCr T measurements performed at 9.2 ± 15.2 mo and 17.4 ± 15.8 mo after onset of PD, respectively, EXCr T did not differ between the first and second study. In patients studied three times and whose fnal assessment occurred 24.7 ± 16.3 mo after initiating PD, EXCr T did not differ between the first and second study, but was significantly lower in the third study compared to the frst study. In patients who were studied four times and whose fourth measurement was taken 31.9 ± 16.8 mo after onset of PD, EXCr T did not differ between any of the studies. The average EXCr T value did not change signifcantly, with the exception of the third study in the patients studied thrice. However, repeated determinations of EXCr T in individuals showed substantial variability, with approximately 50% of the repeated determinations being higher or lower than the first determination by 15% or more.CONCLUSIONThe average value of EXCr T remains relatively constantfor up to 2.5 years of follow-up in PD patients who adhereto the same PD schedule. However, repeated individualEXCr T values vary considerably in a large proportion ofthe patients. Further studies are needed to evaluatethe clinical signifcance of varying EXCr T values and thestability of EXCr T beyond 2.5 years of PD follow-up.