Practice patterns in transitioning patients from chronic kidney disease to dialysis: a survey of United States nephrologists.

BACKGROUND: There are no guidelines for transitioning patients from chronic kidney disease stage 5 to hemodialysis. We conducted this study to determine if there are uniform patterns in how nephrologists transition patients to dialysis. METHODS: We designed an electronic survey with 39 questions and sent it to a database of practicing nephrologists at the National Kidney Foundation. Factors that were important for transitioning a patient to hemodialysis were evaluated, including medication changes on dialysis initiation, dry weight and dialysis prescription. RESULTS: 160 US Nephrologists replied to the survey; 18% (29/160) of the responses were completed via social media sites. Prior to dialysis, 74% (118/160), prescribed furosemide and 67% (107/160) used furosemide with metolazone. Once dialysis started, only 46% (74/160) of the responders continued patients on diuretics daily. Hypertension medications prescribed in dialysis were calcium channel blockers 69% (112/160), beta blockers 36% (58/160), angiotensin converting enzyme inhibitor 32% (53/160), angiotensin receptor blocker 29% (46/160) and diuretics 25% (42/160). Once dialysis started, 68% (109/160) routinely changed medications. Most, 67% (107/160) ordered patients to avoid anti-hypertensive medications on dialysis days to allow for ultrafiltration. Dry weight was determined in the first week by 29% (46/160) and in the first month by 53% (85/160). Most, 59% (94/160) felt that multiple causes lead to hypertension. Most nephrologists would prescribe small dialyzers and a shorter period of time for the first dialysis session. CONCLUSION: The transition period to chronic hemodialysis has variations in practice patterns and may benefit from further studies to optimize clinical practice.

Management of glycemia in diabetic patients with stage IV and V chronic kidney disease.

Diabetic kidney disease is a leading cause of end-stage kidney disease worldwide. Data suggest that prevention of progression to end-stage may lie in excellent blood glucose control; however, as kidney disease progresses, the risk of hypoglycemia increases, due to unpredictable insulin kinetics and altered pharmacokinetics of hypoglycemic agents. In addition, whole classes of hypoglycemic agents become contraindicated and regimens must be adjusted for declining kidney function. There is no consensus regarding the best therapy for the patient with advanced chronic kidney disease. In the best of circumstances, the care of these patients will involve intensive monitoring, with the input of a team of health care providers creating a coordinated care plan, including dietary advice and a drug regimen tailored to the specific issues faced by the individual patient. An open dialogue is necessary at all times, as patients may become frustrated and attempt self-treatment using over the counter alternatives.

Intravenous immunoglobulin in kidney transplantation.

PURPOSE OF REVIEW: Antibody-mediated injury of renal allografts has assumed increasing importance with the availability of potent immunosuppressants directed against T-lymphocytes. Intravenous immunoglobulin (IVIG) has been used for prevention and treatment of antibody-mediated rejection. The review summarizes recent advances that shed light on mechanisms of action of IVIG and outlines current roles of IVIG in kidney transplantation. RECENT FINDINGS: Observational studies support the use of IVIG for desensitization and treatment of acute rejection. Most studies are small and uncontrolled, but a matched case-control study reported a better survival with incompatible live-donor kidney transplant after desensitization using IVIG-containing regimens compared with dialysis or waiting for compatible transplant. Recent data indicate that variations in glycosylation and amino acid sequence cause the crystallizable fragment of immunoglobulin G to assume specific conformations that have high affinity for canonical crystallizable fragment receptors (FcR) or a newly discovered class of FcRs, labelled type II FcRs. Signaling through type II FcRs appears to trigger anti-inflammatory pathways. SUMMARY: Recent discoveries expand our understanding of the mechanism of action of IVIG. Future research is expected to clarify the relevance of these findings to humans and could lead to the development of novel immunomodulatory agents.

Predicting Ionized Hypocalcemia in Critical Care: An Improved Method Based on the Anion Gap.

BACKGROUND: Low ionized calcium (ICa) is prevalent in critical care patients. It is poorly detected by the popular indirect method, which corrects serum total calcium (TCa) for change in albumin. That correction (cTCa) ignores any concomitant change in the anion-complexed fraction of TCa. We tested whether the diagnosis of low ICa can be improved by further correcting for calcium complexation, represented by the anion gap (AG) or its components-sodium, chloride, and total carbon dioxide (tCO2). METHODS: We retrospectively studied all patients in our intensive care units between 2009 and 2011 with ICa measured on arterial (n = 310) or venous (n = 462) gas panels within 19 min of a comprehensive chemistry panel. Logistic models to predict low ICa and linear models to estimate ICa were derived in the arterial group and validated in the venous group, using either AG (AG model) or its components (Ion model) as predictors, adjusted for TCa and albumin. RESULTS: AG and its set of components were each highly significant independent predictors of low ICa. On validation, the logistic Ion model was better than the logistic AG model (ROC curve area ± SE: 0.92 ± 0.02 vs 0.89 ± 0.02; P = 0.008), which, in turn, was far better than cTCa (0.81 ± 0.03; P = 0.0006); the hypocalcemia rates predicted by the models showed good fit with the observed rates. Linear estimates of ICa were too imprecise for clinical use. CONCLUSIONS: The adjustment of TCa for AG or for sodium, chloride, and tCO2 markedly improves the diagnosis of low ICa. This finding may be useful in guiding ICa testing.

Graded interference with the direct potentiometric measurement of sodium by hemoglobin.

OBJECTIVES: Sodium concentration is measured by either indirect (INa) or direct potentiometry (DNa), on chemistry and gas panels, respectively. A spurious difference between these methods (ΔNa=INa-DNa) can be confusing to the clinician. For example, variation in serum total protein (TP) is well known to selectively interfere with INa. Red cells have been suggested to interfere with DNa, but both positive and negative interference have been reported. In this study, the effect of gas panel hemoglobin (Hb) on ΔNa was examined. METHODS: ΔNa was calculated in 772 pairs of closely-timed chemistry and gas panels (median: 4min. apart), retrospectively collected from our critical care units, with 1 pair per patient. Hb was treated as a categorical or continuous variable and tested for linear and non-linear effects, with adjustment for 3 known influences on ΔNa-TP, bicarbonate (tCO2), and the chemistry-gas panel glucose difference (ΔGlu). RESULTS: Hb ranged from 3.5 to 22.0g/dL [35-220g/L]. In categorical analysis, ΔNa increased with Hb, and the effect was essentially linear. By simple regression, ΔNa rose 0.06±0.03[SE]mmol/L per 1g/dL [10g/L] increase in Hb (p<0.05), but confounding was suspected because Hb also correlated (p<10-3) with TP, tCO2, and ΔGlu. Using multiple regression to adjust for the confounders, ΔNa rose 0.15±0.03mmol/L per 1g/dL [10g/L] rise in Hb (p<10-6). CONCLUSIONS: Increasing Hb spuriously decreases DNa and increases ΔNa. A linear correction for this artifact can reduce the discordance between INa and DNa, promoting their interchangeable use.

A hypothesis for mechanism for brain oedema due to glycine.

Death following the use the glycine distension solution in transurethral prostatectomy (TURP) or hysteroscopic surgery has been attributed to the toxic effect of glycine on the brain through the glycine receptors and hyperammonemia, contending that glycine-associated hyponatremia is isosmotic and therefore would not cause brain oedema. Here we propose a hypothesis that the mechanism of brain oedema and death is actually osmotic brain oedema caused by selective diffusion of glycine into the brain while sodium cannot diffuse out of the brain despite favourable concentration gradient because of the absence of sodium transporter on the cerebral capillaries needed for the exit of sodium from the brain. The mechanism for unidirectional diffusion of solutes into the brain in glycine-associated hyponatremia is explained.