Search PubMed⌕ Search

Biomedical subjects

K S Kamel

Publications and source records attributed to K S Kamel.

46 records · Page 3Linked to original sources
PubMed1989

Ammonium excretion in chronic metabolic acidosis: benefits and risks.

The expected renal response to a chronic acid load is an enhanced rate of ammonium production and excretion. Notwithstanding, high rates of ammonium production and/or excretion on a chronic basis may have detrimental consequences to patients. Examples discussed include the loss of extra lean body mass during chronic fasting, an accelerated rate of progression of renal insufficiency and possibly destruction of the medullary area of the kidney owing to local alkalinization.

Acidosis↗
PubMed1989

What is the underlying defect in patients with isolated, proximal renal tubular acidosis?

Our aim in this article is to propose a new hypothesis concerning the etiology of renal tubular acidosis (RTA) in that subgroup of patients who have the isolated, primary type of proximal RTA. We suggest that their underlying disorder is a more alkaline intracellular pH of the proximal convoluted tubule. Increased alkalinity of proximal tubular cells would explain the low rate of bicarbonate reabsorption per liter glomerular filtration and the decreased rate of ammonium excretion despite a low urine pH and the presence of chronic metabolic acidosis. Additional diagnostic tests to evaluate this hypothesis in this specific subgroup of patients with proximal RTA are also outlined.

Acidosis, Renal Tubular↗
PubMed1989

Urine electrolytes in the assessment of extracellular fluid volume contraction.

The purpose of this study was to determine which urine electrolytes should be measured to confirm that the extracellular fluid (ECF) volume is depleted. ECF volume contraction was induced by furosemide administration to rats consuming an electrolyte-free diet. An external potassium balance was achieved by replacing potassium losses with KHCO3 and KCl so that the sodium and chloride deficits were comparable (equivalent to a 30% reduction in ECF volume). As expected, the urine sodium and chloride concentrations fell to 2 +/- 0.3 mmol/l and 3 +/- 0.3 mmol/l, respectively. Rats were then randomized to receive 50-75% of their sodium or chloride deficit as either: NaCl (control group), NH4Cl or NaHCO3 to mimic clinical situations associated with ECF volume contraction. In the NaCl group, the urine sodium and chloride concentrations remained low (6 +/- 2 mmol/l and 7 +/- 2 mmol/l), consistent with persistent ECF volume contraction. Although the NH4Cl group continued to have a low urine sodium concentration (2 +/- 0.2 mmol/l), there was now a marked increase in the urine chloride concentration (51 +/- 7 mmol/l; p less than 0.01 vs. NaCl group). In contrast, although the NaHCO3 group continued to have a low urine chloride concentration (2 +/- 1 mmol/l), there was a significant increase in the urine sodium concentration (19 +/- 3 mmol/l; p less than 0.01 vs. NaCl group). We conclude that the clinical assessment of ECF volume by urine electrolytes requires an evaluation of both the urine sodium and chloride concentrations.

Ammonium Chloride↗
PubMedDate not supplied

An improved approach to the patient with metabolic acidosis: a need for four amendments.

Clinicians should identify life-threatening issues in patients with metabolic acidosis. These threats may be present before therapy begins and/or anticipated after therapy commences. By adding four amendments, short-comings in the commonly used clinical approaches for the diagnosis of metabolic acidosis can be overcome. First, a definition of metabolic acidosis should consider not only the concentration of bicarbonate but also the content of bicarbonate in the extra cellular fluid compartment. The latter requires a quantitative estimate of the ECF volume, which can be obtained using the hematocrit and/or the total protein concentration in plasma. Second, to determine if the basis for metabolic acidosis was the addition of acids or the loss of NaHCO 3 , one must hunt for new anions, not only in plasma, but also in the urine. Third, it is important to measure the venous as well as the arterial PCO2 to assess the capacity to buffer H+ while minimizing H + binding to intracellular proteins. Fourth, to assess the role of the kidney in a patient with metabolic acidosis, the urine osmolal gap and the concentration of creatinine in the urine should be measured to provide an estimate of the rate of excretion of ammonium.

Acid-Base Equilibrium↗