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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2007  |  Volume : 18  |  Issue : 3  |  Page : 430-431
Rhabdomyolysis-Induced Acute Renal Failure in a Patient with Leptospirosis


Nephrology Department, “Evangelismos” General Hospital, Athens, Greece

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How to cite this article:
Droulias J, Moutzouris DA, Kassimatis T, Kollia K, Apostolou T, Hadjikonstantinou V. Rhabdomyolysis-Induced Acute Renal Failure in a Patient with Leptospirosis. Saudi J Kidney Dis Transpl 2007;18:430-1

How to cite this URL:
Droulias J, Moutzouris DA, Kassimatis T, Kollia K, Apostolou T, Hadjikonstantinou V. Rhabdomyolysis-Induced Acute Renal Failure in a Patient with Leptospirosis. Saudi J Kidney Dis Transpl [serial online] 2007 [cited 2020 Sep 19];18:430-1. Available from: http://www.sjkdt.org/text.asp?2007/18/3/430/33765
Renal involvement is common in leptospirosis; and the various manifestations include nonspecific urinary sediment changes, hypokalemia, tubular dysfunction, and acute renal failure (ARF). ARF reflects the severity of leptospirosis and is hyper-catabolic in nature and generally accompanied by cholestatic jaundice and thrombocytopenia. ARF with hyperbilirubinemia represents a severe form of renal dysfunction with oligo-anuria and prolonged clinical course. Mild renal failure is usually anicteric and non-oliguric (rarely requiring dialysis). [1] The pathophysiology of ARF in leptospirosis consists of hypovolemia, direct tubular toxicity, and rhabdomyolysis. We report, herewith, a patient with leptospirosis, severe rhabdomyolysis, and ARF without jaundice or thrombocytopenia. [2]

A 60-year-old man presented with a three­day history of myalgia and gross hematuria and decreased urine output. His medical history included arterial hypertension. Physical examination was unremarkable, except for painful and tense calf muscles. Routine laboratory tests showed serum creatinine (Se Cr) of 6.0 mg/dl, blood urea of 305 mg/dl, sodium of 142 mmol/L, potassium of 6.6 mmol/L, calcium of 9.0 mg/dl, phosphorus of 4.6 mg/dl, and creatine-kinase of 310.507 IU/L. Blood tests revealed leukocytosis (15.2 × 10 3 /µL), without anemia (hematocrit 42.1%) or thrombocytopenia (340 × 10 3 /µL). No obvious cause of rhabdomyolysis was found (e.g., use of statins, macrolides, hypo­thyroidism, etc.). The fractional excretion of sodium was 0.6%, and the urinary excretion of potassium was 590 mmol/day.

The patient required dialysis for 10 days (7 sessions), resulting in decrease in creatine-kinase levels and complete recovery of renal function (Se Cr: 1.0 mg/dl). Urine output was maintained during hospitalization at a mean of 2,000 ml/day. The diagnosis of leptospirosis was confirmed by positive serologic tests (ELISA/IgM). Screening for other infectious diseases (HIV, CMV, Toxoplasma, and Coxsackie) was negative.

The pathophysiology of renal failure in leptospirosis involves all renal structures. Interstitial nephritis is the basic lesion. In addition, there is proximal tubular dysfunction, augmenting distal sodium delivery and potassium excretion by the intact distal tubule. [3] In our case, hyperkalemia was explained by rhabdomyolysis. However, the low fractional excretion of sodium and urinary potassium described in our patient has not been previously reported in literature. In a large series of ARF due to leptospirosis, presented by Covic et al., [4] all patients demonstrated a high fractional excretion of sodium (>1%). Furthermore, 91% of patients with hypokalemia had urinary excretion more than 1,200 mmol/day.

The findings in our case suggest that ARF was caused by rhabdomyolysis per see [5] without the features of tubular dysfunction that is generally seen in leptospirosis­induced ARF. The absence of jaundice, normal platelet count, and low renal excretion of sodium incriminate rhabdomyolysis as the only cause of ARF with no or minimal involvement of leptospirosis. Similar cases have been previously reported in literature, [2],[4],[5],[6] showing that in patients with leptospirosis, ARF could have variable etiology, clinical picture, and laboratory findings.

 
   References Top

1.Visith S, Kearkiat P. Nephropathy in leptospirosis. J Postgrad Med 2005;51(3): 184-8.  Back to cited text no. 1    
2.Coursin DB, Updike SJ, Maki-DG. Massive rhabdomyolysis and multiple organ dys­function syndrome caused by leptospirosis. Intensive Care Med 2000;26:808-12.  Back to cited text no. 2    
3.Magaldi AJ, Yasuda PN, Kudo LH, Seguro AC, Rocha AS. Renal involvement in leptospirosis: a pathophysiologic study. Nephron 1992;63:332-9.  Back to cited text no. 3    
4.Covic A, Goldsmith DJ, Gusbeth-Tatomir P, Seica A, Covic M. A retrospective 5­years study in Moldova of acute renal failure due to leptospirosis: 58 cases and review of the literature. Nephrol Dial Transplant 2003; 18:1128-34.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Corwin HL, Schreiber MJ, Fang LS. Low fractional excretion of sodium. Occurrence with hemoglobinuric- and myoglobinuric­induced acute renal failure. Arch Intern Med 1984;144:981-2.  Back to cited text no. 5    
6.Liborio AB. Can rhabdomyolysis be the only cause of acute renal failure in leptospirosis? Nephrol Dial Transplant 2005;20(11):2580-1.  Back to cited text no. 6    

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Correspondence Address:
John Droulias
Nephrology Department, “Evangelismos” General Hospital, Athens
Greece
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PMID: 17679759

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