Factors that affect albumin concentration in dialysis patients and their relationship to vascular disease

Factors that affect albumin concentration in dialysis patients and their relationship to vascular disease.IntroductionHypoalbuminemia is a powerful risk factor for cardiovascular mortality in hemodialysis patients (HD). Inflammation causes a decrease in albumin synthesis and an increase in albumin fractional catabolic rate, providing two mechanisms for hypoalbuminemia. The inflammatory response alters the endothelium and plasma protein composition in ways that favor vascular injury. Plasma volume is expanded in HD patients, providing another mechanism for hypoalbuminemia. Fibrinogen levels are an independent risk factor for cardiovascular disease (CVD) in HD patients, and fibrinogen levels are increased in HD patients. Plasma volume expansion is also an independent risk factor for CVD.MethodsAlbumin synthesis was measured in 74 HD patients as the disappearance of [125I] human albumin over six weeks. Fibrinogen was measured in plasma. Plasma fibrinogen mass was the product of fibrinogen concentration and plasma volume.ResultsAlbumin synthesis correlated positively with plasma volume (P < 0.001). Fibrinogen concentration and plasma fibrinogen mass both correlated positively with albumin synthesis (P < 0.001).ConclusionAlbumin levels are reduced as part of the acute-phase response in HD. Plasma volume expansion also tends to decrease albumin concentration, but elicits an increase in its rate of synthesis, which, in turn, is associated with increased fibrinogen levels. Thus, both inflammation and plasma volume expansion factors that reduce albumin concentration and are independent cardiovascular risk factors, independently increase fibrinogen levels

Early pre-eclampsia unmasks underlying IgA nephropathy

Mona Singh, Akhenaton Pappoe, Burl R DonDivision of Nephrology, University of California Davis Medical Center, Sacramento, CA, USAAbstract: Pre-eclampsia is the most ominous complication of pregnancy, and primary glomerular diseases can mimic pre-eclampsia in presentation. A patient presented at 21 weeks gestation with signs and symptoms of both pre-eclampsia and primary glomerular nephropathy. A critical clinical decision whether to continue or terminate the pregnancy was dependent on results of a renal biopsy. The biopsy noted the presence of both pre-eclampsia and immunoglobulin A (IgA) nephropathy. Thus, the onset of pre-eclampsia unmasked the presence of unrecognized IgA nephropathy, and the IgA nephropathy was a risk factor for this patient developing pre-eclampsia. The results of a renal biopsy are key in distinguishing pre-eclampsia from other kidney diseases and instituting appropriate clinical management.Keywords: proteinuria, IgA nephropathy, renal biopsy, pre-eclampsi

Nutritional and Non-nutritional Management of the Nephrotic Syndrome

[No abstract available

Thin-glomerular-basement-membrane nephropathy: is it a benign cause of isolated hematuria?

Thin-glomerular-basement-membrane (TGBM) nephropathy is among the most common causes of isolated hematuria. This autosomal dominant disorder is characterized by diffuse thinning of the GBM and is diagnosed by electron microscopic examination of renal biopsy tissue. A study of an affected kindred has revealed a mutation in the alpha chain of type IV collagen, resulting in abnormal basement membrane synthesis. Although the exact prevalence and prognosis is unclear, TGBM is usually regarded as a benign cause of hematuria and not associated with any untoward effect on renal function. We report a case of TGBM nephropathy, with associated proteinuria and progressive renal insufficiency. Other studies similarly contend that TGBM nephropathy may not be so benign. On the basis of these findings, we suggest that in some patients with TGBM nephropathy, progressive renal insufficiency may develop. We recommend a more vigilant approach in patients with TGBM nephropathy, especially if proteinuria is present

Successful treatment of renal amyloidosis due to familial cold autoinflammatory syndrome using an interleukin 1 receptor antagonist

Familial cold autoinflammatory syndrome (FCAS) is an autosomal dominant disorder characterized by episodic fever, arthralgias, conjunctivitis, and rash triggered by cold exposure. FCAS is rarely associated with progressive renal insufficiency caused by renal amyloidosis. The genetic defect in patients with this disorder is caused by a mutation in the gene encoding the protein cryopyrin, leading to uninhibited activation of systemic inflammation through specific cellular signaling with increased production of a number of key cytokines, including interleukin 1. We describe the successful treatment of a patient with renal amyloidosis caused by FCAS by using a novel interleukin 1-receptor antagonist. Use of specific anticytokine therapy may be a new paradigm in the treatment of patients with renal amyloidosis caused by systemic inflammatory diseases

Building a hemodiafiltration system from readily available components for continuous renal replacement therapy under disasters and pandemics: preparing for an acute kidney injury surge during COVID-19.

Purpose of reviewThe novel corona virus (SARS-CoV2) has been demonstrated to cause acute kidney injury due to direct cellular toxicity as well as due to a variety of autoimmune glomerular diseases. The concept of a surge of infected patients resulting in an overwhelming number of critical patients has been a central concern in healthcare planning during the COVID-19 era.Recent findingsOne crucial question remains as to how to manage patients with end stage renal disease and acute kidney injury in case of a massive surge of critically ill infected patients. Some publications address practical and ingenious solutions for just such a surge of need for renal replacement therapy. We present a plan for using a blood pump, readily available dialysis filter, and a prefilter and postfilter replacement fluid set up. This is in conjunction with multiple intravenous pumps to develop a simple hemofiltration apparatus.SummaryThe current set up may be a readily available option for use in critical situations where the need for renal replacement therapy outstrips the capacity of traditional hemodialysis services in a hospital or region

Tentative pavement and geometric design criteria for minimizing hydroplaning. Phase I. Final report.

Federal Highway Administration, Office of Research and Development, Washington, D.C.Mode of access: Internet.Author corporate affiliation: Texas Transportation Institute, College StationSubject code: CGSubject code: MSDSubject code: NCXCSubject code: NCYS*CDFSubject code: NHDHHSubject code: NVSSubject code: WNBSubject code: WOB*

Severe hypercalcemic hyperparathyroidism developing in a patient with hyperaldosteronism and renal resistance to parathyroid hormone.

We evaluated an African American woman referred in 1986 at age 33 years because of renal potassium and calcium wasting and chronic hip pain. She presented normotensive, hypokalemic, hypocalcemic, normophosphatemic, and hypercalciuric. Marked hyperparathyroidism was evident. Urinary cyclic adenosine monophosphate (cAMP) excretion did not increase in response to parathyroid hormone (PTH) infusion, indicating renal resistance to PTH. X-rays and bone biopsy revealed severe osteitis fibrosa cystica, confirming skeletal responsiveness to PTH. Renal potassium wasting, suppressed plasma renin activity, and elevated plasma and urinary aldosterone levels accompanied her hypokalemia, suggesting primary hyperaldosteronism. Hypokalemia resolved with spironolactone and, when combined with dietary sodium restriction, urinary calcium excretion fell and hypocalcemia improved, in accord with the known positive association between sodium intake and calcium excretion. Calcitriol and oral calcium supplements did not suppress the chronic hyperparathyroidism nor did they reduce aldosterone levels. Over time, hyperparathyroid bone disease progressed with pathologic fractures and persistent pain. In 2004, PTH levels increased further in association with worsening chronic kidney disease. Eventually hypercalcemia and hypertension developed. Localizing studies in 2005 suggested a left inferior parathyroid tumor. After having consistently declined, the patient finally agreed to neck exploration in January 2009. Four hyperplastic parathyroid glands were removed, followed immediately by severe hypocalcemia, attributed to "hungry bone syndrome" and hypoparathyroidism, which required prolonged hospitalization, calcium infusions, and oral calcitriol. Although her bone pain resolved, hyperaldosteronism persisted