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| Year : 2009 | Volume
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| Issue : 5 | Page : 850-851 |
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| Acute urate nephropathy precipitated by acute diarrhea |
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Wael Latif Jabur
New Medical Center Specialty Hospital P.O. Box 7832, Dubai, United Arab Emirates
Click here for correspondence address and email
| Date of Web Publication | 2-Sep-2009 |
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How to cite this article:
Jabur WL. Acute urate nephropathy precipitated by acute diarrhea. Saudi J Kidney Dis Transpl 2009;20:850-1 |
To the Editor,
One of the common difficulties encountered in clinical nephrology is to differentiate pre-renal azotemia from intrinsic acute renal failure (ARF). A definitive diagnosis can be made by kidney biopsy, but is seldom indicated in patients with ARF secondary to under perfusion or profound renal ischemia. The same controversy is relevant for the diagnosis of the acute crystal nephropathy, and in particular ARF secondary to acute urate nephropathy, a condition in which there is hyperuricemia, usually secondary to tumor lysis syndrome or rhabdomyolysis. We herewith report on a 55-year-old male patient who presented with a history of diarrheal illness of one weeks duration. The frequency of loose stools was more than 20 times per day, it was watery, voluminous, non-bloody and was not associated with abdominal pain, nausea or vomiting. There was no history of fever or travel abroad. The diarrhea resulted in hypovolemia and oliguria for two days prior to admission to the intensive care unit of our hospital. Ultrasound of the kidney showed kidneys of normal size and texture with no obstruction. He had no prior history of kidney disease, diabetes mellitus, hypertension or hyperuricemia.
Blood parameters at admission revealed hyperuricemia of 15.5 mg/dL, serum potassium of 3.8 meq/L, serum creatinine of 7.5 mg/dL, 24-hr urine uric acid of 285 mg/day and glomerular filtration rate (GFR) of 14 mL/min. The 24hour urinary creatinine was 1050 mg/ day. The urine sodium concentration was 80 mmol/L, fractional excretion of sodium was 1.1% and specific gravity was 1.035. Urine uric acid to creatinine ratio was 0.25. Fractional excretion of uric acid was 13%. The patient's urine output improved gradually with prompt fluid replacement and kidney function normalized after one month with conservative management only.
Several intriguing issues arise in the context of this patient's illness including:
- is it possible for advanced acute kidney injury (AKI) (RIFLE class 3) to be solely hemodynamically mediated?;
- is it possible for severe hyperuricemia to be precipitated by ARF?; and
- is it possible for acute urate nephropathy to be provoked by primary idiopathic hyper uricemia?
It is still debatable as to how one can prove that the ARF is secondary to acute urate nephropathy without histopathological evidence. All the features reported in the literature for this diagnosis present many evidences without any strong conclusion. The most widely recognized presentation is the occurrence of oliguric ARF in the presence of hyperuricemia of more than 15 mg/dL, urinary uric acid of 150-200 mg/dL, and urinary uric acid to creatinine ratio of more than one. [1]
In our patient, although the urine specific gravity and urate to creatinine ratio were indicative of pre-renal failure rather than acute urate nephropathy, the high serum creatinine which conformed to stage 3 AKI on RIFLE classification, [2] would suggest significant underlying structural damage. Also, the high fractional excretion of sodium is consistent with a diagnosis of acute tubular necrosis (ATN).
The RIFLE classification does not include the underlying pathological condition that could explain the severity of renal failure; [2] however, the oliguric state that followed the severe diarrheal illness, followed by prompt resumption of diuresis after adequate fluid replacement would denote acute pre-renal failure due to under perfusion. However, the gradual improvement of GFR over one month combined with fractional excretion of sodium of more than 1%would suggest the existence of ATN. Additionally, the high levels of serum uric acid would concur with the diagnosis of ATN and would propose a critical role for uric acid in its pathogenesis. Such high levels of serum uric acid (more than 15 mg/dL) is seldom a result of renal failure. [3] It is well recognized that the hyperuricemia correlates with the degree of renal impairment and it peaks in parallel to the reduction of GFR. This is particularly so in the case of acute pre-renal failure, where due to avid proximal tubular reabsorbtion, urinary excretion of uric acid would be scanty. In our patient, the severity of hyperuricemia cannot be explained solely by renal failure; also, the marked hyperuricosuria (fractional excretion of uric acid of 13%) is not consistent with pre-renal etiology. [4] Despite the fact that the urinary uric acid level was less in the early phase, it was relatively high for the level of GFR; this could be the reason why the fractional excretion of uric acid was higher than normal (13%) during the phase of renal failure than during the recovery phase, and the ratio of urinary uric acid to GFR was higher with a GFR of 14 mL/min, than with a GFR of 50 mL/min. This is indicative of increased uric acid excretion during the period of renal shut down. This would highlight the probability that the hyperuricemia is the cause (at least partly) of the ARF and not the result. Nonetheless, it is unusual for acute urate nephropathy to be precipitated by idiopathic primary hyperuricemia, [3] because of the fact that in the majority of the patients, the underlying pathology is the inherent renal uric acid underexcretion. [5] Also, in the absence of evidence for increased production of uric acid such as blood dyscrasias, lymphoproliferative disorders, tumor lysis syndrome and rhabdomyolysis, which are the most common circumstances with which acute urate nephropathy is associated, secondary hyperuricemia is unlikely. [6] The hyperuricemia might be explained by genetically determined overproduction that became evident due to plasma contraction. Although the immediate improvement of urine output might be explained by the reversible functional vasoconstrictive property of hyperuricemia, it would also negate the probability of massive acute kidney injury. [3],[7]
The fractional excretion of uric acid in combination with fractional excretion of sodium would prove explicitly that urate nephropathy is the cause of ARF in our patient even with normal uric acid to creatinine ratio.
 References | |  |
| 1. | Cameron JS, Moro H, Simmonds HA. Uric Acid and the kidney. In: Oxford Textbook of Clinical Nephrology, Davison AM, Cameron S, Grunfeld JP (eds). 2nd edn. Oxford, University Press, 1998;pp 1159-73.  |
| 2. | Melnikov VY, Molitoris BA. Improvements in the diagnosis of acute kidney injury. Saudi J Kidney Dis Transpl 2008;19(4):537-44. |
| 3. | Ahsan Ejaz A, Mu W, Kang DH, et al. Could uric acid have a role in acute renal failure? Clin J Am Soc Nephrol 2007;2:16-21 |
| 4. | Massayoshi S, Yukio H. Serum uric acid level and fractional excretion in fluid and electrolyte disturbances. Jpn J Clin Pathol 1999;47(5):417-23. |
| 5. | Dincer HE, Dincer AP, Levinson DJ. Asymptomatic hyperuricemia: To treat or not to treat. Cleveland Clin J Med 2002;69(8):594-607. |
| 6. | Ronco C, Inguggiato P, Bordoni V, et al. Rasburicase therapy in acute hyperuricemia and renal dysfunction. Contrib Nephrol 2005;147: 115-23. |
| 7. | Kim YG, Huang XR , Suga S, et al. Involvement of macrophage migration inhibitory factor (MIF) in experimental uric acid nephropathy. Mol Med 2000;6:837-48. [PUBMED] [FULLTEXT] |
Correspondence Address:
Wael Latif Jabur
New Medical Center Specialty Hospital P.O. Box 7832, Dubai
United Arab Emirates
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PMID: 19736489 
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