Volume 6 Issue 4, April 2010

The abstract of the RENAL Replacement Therapy study concludes that in critically ill patients with acute kidney injury, treatment with higher-intensity continuous renal replacement therapy did not reduce mortality. However, the real news is that survival and recovery of renal function might depend on how therapy is provided.

Are selective endothelin-receptor antagonists really an important new advance for treating patients with treatment-resistant hypertension? The evidence from a recent study leaves us with some uncertainty.

Blockade of the renin–angiotensin system has beneficial effects in patients with diabetic nephropathy; however, this treatment can induce aldosterone breakthrough and thus become ineffective. New data indicate that aldosterone breakthrough develops even when maximal doses of an angiotensin-converting-enzyme inhibitor are administered to patients with diabetic nephropathy.

Autosomal dominant polycystic kidney disease (ADPKD) is a common nephropathy caused by mutations in eitherPKD1 or PKD2. Molecular analyses are increasingly used for the diagnosis of this disease and are particularly helpful when imaging studies are equivocal and a definite diagnosis is required. In this Review, Harris and Rossetti discuss the role of molecular diagnostics in ADPKD and describe the different approaches that are used. Genetic complexities that require consideration when using molecular diagnostics in ADPKD are also described.

Phosphate is critical for the maintenance of skeletal integrity, is a necessary component of important biomolecules, and is essential for cellular metabolism. Mechanisms of phosphate regulation in the kidney—the most critical organ for maintaining short-term serum phosphate concentrations—are incompletely understood. This Review describes how the identification of genetic alterations in Mendelian disorders of hypophosphatemia and hyperphosphatemia has led to the isolation of novel genes and the identification of new roles for existing proteins in the control of renal phosphate handling.

A wide range of erythropoiesis-stimulating agents to stimulate red blood cell production are currently in clinical use, but advances in our understanding of erythropoiesis have provided an ever-increasing array of potential therapeutic targets. Here, Robert Foley describes the desirable properties of erythropoiesis-stimulating agents and discusses various novel agents currently under assessment for the treatment of anemia in patients with chronic kidney disease. Such agents include proteins and peptides that activate erythropoietin receptors, non-protein agents, and strategies with targets other than erythropoietin receptors.

Toll-like receptors (TLRs) have a key role in the regulation of innate immunity by mediating signal transduction pathways that modulate the expression of proinflammatory cytokines and chemokines. This Review discusses the potential role of TLRs in the pathogenesis of renal conditions such as acute kidney injury, acute glomerulonephritis, and renal transplant rejection. The authors also describe studies that have used pharmacological inhibition of TLR signaling to modify the response to proinflammatory stimuli.

This article reports the case of a 36-year-old man on hemodialysis who presented to an intensive care unit with a large serum anion gap and symptoms such as hypotension and an altered mental state. For the previous 6 weeks, he had received linezolid to treat vancomycin-resistant bacteremia. Discontinuation of linezolid led to resolution of his symptoms and to normalization of the serum anion gap and serum lactate levels. The authors conclude that the patient had suffered from lactic acidosis caused by linezolid.