Paralysis due to renal potassium wasting: an unusual presentation of leptospirosis

Anand Krishnan, Dilip R. Karnad and Tushar P. Medhekar

Medical-Neurology Intensive Care Unit Department of Medicine King Edward Memorial Hospital Parel, Mumbai 400 012 India Email: docandy22{at}hotmail.com

Sir,

Case. A 43-year-old male was admitted to hospital 16 h after onset of myalgia, progressive quadriparesis, respiratory muscle weakness and dysphagia. He was conscious, with a pulse of 120/min, BP 120/70 mmHg and tachypnoeic, and had conjunctival suffusion, flaccid hyporeflexic weakness and flexor plantar responses. Sensations were normal and meningeal signs absent. He had abdominal distension with absent bowel sounds.

Arterial blood showed mixed respiratory and metabolic acidosis with a pH of 7.20, pO2 60 mmHg, pCO2 46 mmHg, oxygen saturation 92% and bicarbonate 17.6 mmol/l. The serum sodium was 140 mmol/l, potassium 2.6 mmol/l, chloride 116 mmol/l and blood urea nitrogen (BUN) 12 mg/dl. He was endotracheally intubated and mechanically ventilated. Following i.v. correction of hypokalaemia, serum potassium improved to 3.6 mmol/l and the patient was weaned off the ventilator and extubated within 12 h.

Investigations revealed BUN 25 mg%, serum creatinine 1.2 mg% and normal liver function, total leukocyte count (TLC) and platelet counts. The urine pH was 5.22, urine potassium 27.9 mmol/l, sodium 23.2 mmol/l, chloride 54.8mmol/l, urine osmolality 351 mOsm/kg, plasma osmolality 294 mOsm/kg and total urine volume 4500 ml. The arterial pH at this time was 7.28 and bicarbonate 17.6 mmol/l. The normal anion-gap metabolic acidosis and transtubular potassium gradient >5 suggested renal tubular dysfunction with potassium wasting.

Forty-eight hours later, the patient developed high fever and oliguria. He now had severe muscle tenderness, icterus and increased conjunctival suffusion. BUN had increased to 77 mg% and serum creatinine to 2.7 mg%. Total bilirubin was 21.6 mg% (direct: 15.3 mg%), SGOT (AST) 191 U/l, SGPT (ALT) 96 U/l, sodium 138.0 mmol/l, potassium 3.6 mmol/l and chloride 108.0 mmol/l. Platelet counts dropped to 60 x 109/l and TLC increased to 13.9 x 109/l with 85% polymorphonuclear cells. Abdominal ultrasonography showed normal liver and enlarged kidneys (right: 12.6 x 4 cm; left: 12.2 x 4.1 cm). A diagnosis of leptospirosis was considered, as an epidemic was raging in the city at this time. He was treated with crystalline penicillin (1^ 500^ 000 IU every 6 h) and recovered over the next 5 days without needing dialysis. Leptospirosis was confirmed by the presence in serum of IgM antibodies (1 : 50) against the heat-stable antigen of Leptospira biflexa (Lepto Dipstick; Organon Technika Ltd, Dublin, Irish Republic).

Comment. Renal involvement in the form of interstitial nephritis and tubular necrosis is common in leptospirosis [1,2]. Leptospires reside in the proximal tubules [3], which are maximally affected [1,2]. Yang et al. [2] showed that the proximal tubular dysfunction may be restricted to the Na+-H+ antiporter-mediated process. The thick ascending limb of the loop of Henle also could be affected in some patients, especially those with severe jaundice [4]. The resulting abnormal sodium and chloride transport place an increased load of sodium on the distal tubule, which is relatively unaffected, resulting in impaired reabsorption of potassium [1,2]. Hypokalaemia may therefore occur, even in patients with significant azotaemia [5]. Though the negative urinary anion gap and urinary pH <5.5 in our patient suggest proximal renal tubular dysfunction, the relatively less negative urinary anion gap points to defective ammonium excretion as well.

In conclusion, leptospirosis must be considered in patients presenting with symptomatic hypokalaemia, especially in endemic areas. Four months after the admission of the here reported case, another patient with leptospirosis presented with hypokalaemic quadriparesis and manifested hepatic and renal dysfunction 3 days later, suggesting that this form of presentation may not be as rare as is believed.

Acknowledgments

We thank Dr Alan F. Almeida for his valuable suggestions regarding the manuscript.

Conflict of interest statement. None declared.

References

  1. Lomar AV, Diament D, Torres JR. Leptospirosis in Latin America. Inf Dis Clin North Am 2000;14: 23–39[ISI]
  2. Yang CW, Pan MJ, Wu MS et al. Leptospirosis: an ignored cause of acute renal failure in Taiwan. Am J Kidney Dis 1997;30: 840–845[ISI][Medline]
  3. Thomson JC, Marktelow BW. Pathogenesis of renal lesions in hemoglobinaemia and non-hemoglobinaemic leptospirosis. J Comp Pathol 1989;101: 201–214[ISI][Medline]
  4. Lin CL, Wu MS, Yang CW, Huang CC. Leptospirosis associated with hypokalaemia and thick ascending limb dysfunction. Nephrol Dial Transplant 1999;14: 193–195[Abstract]
  5. Seguro A, Lomar A, Rocha A. Acute renal failure of leptospirosis: nonoliguric and hypokalemic forms. Nephron 1990;55: 146–151[ISI][Medline]




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