Ankit N. Mehta

GOLD MARK: an anion gap mnemonic for the 21st century.

892 www.thelancet.com Vol 372 September 13, 2008 have posed and answered these key questions. But after the trials, what next? English hospitals reported more procedures for abdominal aortic aneurysm repair, with higher operative mortality (8·7%) than fi gures reported by the National Vascular Database (6·8%). A national registry could easily be useless if practitioners submit only good results. Making the funding of devices conditional on entry to the national register is a start, but more is required. To emulate the excellent result from these trials, a similar learning curve, interdisciplinary working, and selection for procedure should be required as conditions of funding. A national registry could indeed be a major asset once key questions are settled by randomised controlled trials. The link of mandatory registration and mandatory protocol within the register is the key to the achievement of best practice. Both randomised controlled trials and national registries are needed for new interventional procedures.

Current opinions in renovascular hypertension

Renal artery stenosis and renovascular hypertension are important considerations in patients with hypertension that is difficult to control. The diagnosis may also have prognostic significance for progressive renal disease. The most common causes of renal artery stenosis are atherosclerotic disease and fibromuscular dysplasia. The pathophysiology of renal artery stenosis is reviewed, and the pros and cons of various imaging studies in the appropriate clinical setting are discussed. Treatment includes aggressive control of hypertension, dealing with associated cardiac risk factors, and angioplasty or surgery in specific circumstances.

Hyperammonemic syndrome after Roux-en-Y gastric bypass

Hyperammonemic encephalopathy is an uncommon but severe complication of the Roux‐en‐Y gastric bypass surgery for obesity. Mechanisms underlying this complication are incompletely understood, resulting in delayed recognition and management. This study evaluated common laboratory findings and possible etiology of hyperammonemic encephalopathy after successful Roux‐en‐Y gastric bypass surgery.

Gastrointestinal potassium binding–more than just lowering serum [K+]: patiromer, potassium balance, and the renin angiotensin aldosterone axis

Hyperkalemia limits the use of renin-angiotensin-aldosterone axis (RAAS) blockers in patients with renal insufficiency. This can be managed by efforts to increase kaliuresis and by gastrointestinal potassium binding with sodium polystyrene sulfonate, a relatively ineffective agent. Now with the availability of patiromer, RAAS blockers can be used more liberally. In addition, potassium reduction decreases aldosterone, which may be beneficial. Adverse nonepithelial aldosterone effects such as endothelial dysfunction and cardiac fibrosis may be ameliorated.

Multiple myeloma presenting as acute renal failure

Multiple myeloma is a plasma cell dyscrasia that can have various clinical presentations. Signs and symptoms often reflect plasma cell infiltration into organs but can be subtle. We report a case of a woman who presented with nonoliguric acute kidney injury as the initial manifestation of multiple myeloma.

The Importance of a “Just Right” Serum Potassium Level

Ion pumps energized by ATP, such as Na-K ATPase, together with a multitude of ion channels and transporters that exist in cell membranes generate ion concentration gradients, which then result in cellular transmembrane electrical gradients. The potassium gradients between cellular and ECF spaces are particularly important in this regard. These electrical gradients are critical for the appropriate functioning of central and peripheral nerve cells, cardiac conducting tissues and contraction of all muscle cells. As a result, both hypo and hyper kalemia are especially dangerous electrolyte disorders because of the many adverse effects they generate in muscle, nerves and cardiac electrical activity. Whole body potassium homeostasis is achieved by the quantitative renal excretion of ingested potassium. Therefore, acute kidney injury and chronic kidney diseases (CKD) with the resultant fall in glomerular filtration and tubule function are important causes of hyperkalemia. These disorders may originate in the kidneys or the abnormalities may be the result of primary cardiovascular pathology. Another increasingly common cause of hyperkalemia is the therapeutic use of inhibitors or blockers of the renin-angiotensin-aldosterone system – angiotensin converting enzyme inhibitors, angiotensin receptor Referring to the composition of extracellular fluid (ECF), Claude Bernard stated: “The fixity of the milieu supposes a perfection of the organism such that the external variations are at each instant compensated for and equilibrated....” [1] . The “normal” or “reference” range for each of the ions and molecules dissolved in mammalian ECF has evolved over many millions of years. Persistently increased or decreased concentrations of virtually any of these ions/molecules are generally associated with a disease or disorder and often predict increased risk of morbidity and/or mortality. These risk increases are related to both the inherent risk of underlying diseases and disorders that have generated the chemical or biochemical abnormalities and also because, in many cases, the abnormal concentration of the ion or molecule can directly generate additional pathology. In the case of the routinely measured plasma electrolytes: sodium, potassium, chloride and bicarbonate, many studies, across a wide spectrum of diseases and settings, have demonstrated that either high or low values increase morbidity and mortality risk. Thus, the morbidly or mortality risk plotted against ion concentration results in a “U”, “J” or reverse “J” shaped risk profiles. In this regard, the serum potassium concentration is a particularly pernicious analyte. Published online: September 2, 2017 Nephrology American Journal of

Patiromer-an Oral Calcium-Loaded Potassium Binder: Kalirrhea with Calciuresis.

In the absence of diarrhea, about 90% of ingested potassium (K) is absorbed and excreted into the urine. Renal K excretion is impaired by a marked reduction in kidney function, kidney disorders, or drugs which sharply reduce the distal tubular delivery of sodium and/or reduce the renal tubular