Thiazides, metolazone and loop diuretics were absent in her urine. Our patient did not report constipation (which might have induced her to ingest excessive alkali) or chronic diarrhoea with persistent (Na or K) chloride losses. NaHCO 3) or that non-renal loss of chloride occurred. This finding suggests that either the patient ingested other sodium salts (e.g. Most of the dietary intake of sodium was not in the form of sodium chloride, as twice as much sodium was excreted as compared to chloride. Her 24-h urinary potassium excretion was high, about twice the daily excretion expected in Germany. Our patient presented with hypokalaemia, metabolic alkalosis and a normal blood pressure. Calcifications were also identified in the tubular epithelial cells (Figure (Figure2 2). Heavy interstitial calcifications were observed in the cortex and outer medulla (Figure (Figure1). However, the interstitium showed round cell infiltrate and matrix expansion. A kidney biopsy revealed normal glomeruli and blood vessels. Renal ultrasound revealed normal-sized kidneys with increased cortical density and a suggestion of nephrocalcinosis. Urine was tested for diuretic metabolites of furosemide, hydrochlorothiazide, mefruside, piretanide, xipamide and canrenone, but none were found. A 1,25-hydroxyvitamin D level was normal, while the parathyroid hormone concentration was 121 pg/ml (10–65 pg/ml). The renin/aldosterone ratio was 9.4 (normal <50). The sediment was bland, and modest proteinuria (368 mg/24 h albumin 275 mg/24 h, IgG 15 mg/24 h, alpha-1 microglobulin 35 mg/24 h) was present. A urine specimen showed an alkaline pH 8.5. The haemoglobin was 11 g/dl the gamma-glutamyl transferase was slightly elevated at 86 U/l, while other liver enzymes were normal. The calcium excretion was lower than expected, while the magnesium excretion was normal. The finding strongly suggests that most of the cation secretion was ingested with some anion other than chloride. The urine anion gap (-UCl) was 200 mmol in a 24-h collection.
The chloride excretion was substantially lower than the cation excretion. Notable are the slightly reduced chloride concentration and the high urine sodium and potassium excretion. The electrolyte values are given in Table Table1. Her pH was 7.59, PaCO 2 30 mmHg and HCO 3 29 mmol/l. Her creatinine concentration was 1.8 mg/dl, estimated glomerular filtration rate was 33 ml/min and the potassium was 3.3 mmol/l. She had tooth decay, but no inner enamel loss. Her volume status was normal, there was no oedema and the organ systems were intact. The body mass index was 24.7 kg/m 2, the blood pressure was 130/70 mm Hg and the heart rate was 72 beats/min without orthostatic changes. She was divorced but lived in a stable relationship. The patient expressed concern about her weight but denied bulimia, vomiting induction, laxative or diuretic abuse. She had abused alcohol as an adult and had several earlier admissions for withdrawal and counselling. As a child, the patient had been obese and had been sent to a weight loss centre that resulted in a 15 kg weight reduction. A high alcohol intake with complications was suspected but could not be proved. An elevated creatinine concentration (3 mg/dl) and hypokalaemia (3.0 mmol/l) were recorded. We recently encountered a patient who taxed our diagnostic skills.Ī 42-year-old woman was first seen in our hospital with ‘hyperventilation and panic attacks’. Diuretic abuse may be a confounder however, metabolic breakdown products and the temporal course of chloride excretion generally solve the mystery. In patients with high urinary potassium with metabolic alkalosis, the urinary chloride concentration can be particularly helpful in separating surreptitious vomiting from Bartter's syndrome or Gitelman's syndrome. In any event, acid–base status is extremely helpful and generally indicates which end of the gastrointestinal tract or which level of the nephron is responsible. In patients with a high urinary potassium excretion, the kidneys themselves are implicated. In those patients with low urinary potassium excretion, a gastrointestinal cause for the hypokalaemia would come to mind. Diagnostic steps usually involve assessing urinary potassium excretion, transtubular potassium gradient (TTKG) and concomitant acid–base disturbances. History and physical examination can be misleading or inaccurate.
Unravelling chronic hypokalaemia can be a clinical challenge in some patients.
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