Anatol J Clin Investig 2013;7(4):225-227
A RARE CAUSE OF POST-EXERCISE ACUTE RENAL FAILURE: RENAL HIPOURICEMIA EGZERSİZ SONRASI AKUT BÖBREK YETMEZLİĞİNİN NADİR BİR NEDENİ: RENAL HİPOÜRİSEMİ Hilmi Umut ÜNAL1, Mustafa ÇAKAR2, Mahmut GÖK1, Mahmut İlker YILMAZ1, Tayfun EYİLETEN1, Kayser ÇAĞLAR1, Yusuf OĞUZ1 1 1
GATA, Nefroloji BD., Ankara. GATA, İç Hastalıkları AD., Ankara.
Abstract Acute renal failure is a rarely occurring condition after any effort or an intensive exercise program. One of the reasons of kidney failure occurring after an exercise is renal hipouricemia. Idiopathic renal hipouricemia is a genetic disease and is characterized by abnormal renal tubular excretion of uric acid. We here present a case of a 36-year-old man suffering acute renal failure occurring after an exercise. Key words: Kidney failure, renal hypourisemia, exercise. Özet Yoğun bir egzersiz programı veya efor sonrası akut böbrek yetmezliğinin ortaya çıkması nadir bir durumdur. Egzersizin yol açtığı böbrek yetmezliğine yol açan nedenlerden biri de renal hipoürisemidir. İdiyopatik renal hipoürisemi genetik bir hastalık olup normalin üstünde renal tubuler ürik asit atılımı ile ortaya çıkar. Biz burada egzersiz sonrası tekrarlayan akut böbrek yetmezliği tablosu ile başvuran 36 yaşında erkek bir olguyu sundu. Anahtar kelimeler: Böbrek yetmezliği, renal hipoürisemi, egzersiz.
Introduction Acute renal failure following an exercise usually develops due to massive rhabdomyolysis. Flank pain, elevated serum creatine phosphokinase and myoglobin values with acute renal failure may also develop after an intensive exercise [1]. Idiopathic renal hypouricemia is a genetic disease characterized by decreased serum levels and increased renal excretion of uric acid [2]. Acute renal failure after an exercise associated with renal hypouricemia was first described in 1989 in a 23 year old male patient with advanced renal insufficiency to require hemodialysis [3]. Most of the cases have been reported from Japan, and the incidence varies between 0.12% 0.72%. Most patients are asymptomatic but may present with complications in the form of nephrolithiasis or acute renal failure after an exercise [4,5]. Case 36 year old male patient was admitted with complaints of recurrent nausea and vomiting after an intensive exercise. The current complaints repeated two times in the last 4 months. On the first admission, serum creatinine of the patient was 8 mg/dL and urea was 106 mg/dL. With a possible diagnosis of acute renal failure, patient was hydrated and when serum creatinine decreased to 1.2 mg/dL, he was discharged. 2
months later, after an intensive exercise program, he again had complaints of nausea and vomiting. Laboratory values on the admission were as follows: hemoglobin: 13.1 g/dL, hematocrit: 35.5%, platelet: 270000/μL, leukocyte: 8240/mL, serum creatinine: 3.23 mg/dL, urea: 46 mg/dL, serum glucose: 89.4 mg/dl, serum sodium: 139 mEq/l, serum potassium: 4:38 mEq/l, serum chloride: 108.8 mEq/l, AST: 16.93 IU/l, creatine kinase: 362 IU/l, serum uric acid: 0.6 mg/dl, 24hour urinary uric acid: 8.3 mg/dl. Bilateral renal ultrasound imaging was considered to be normal. After hydration of the patient, serum creatinine value decreased to the normal range and was discharged. In follow-up of the patient for recurrent acute renal failure following exercise, serum creatinine was measured as 0.82 mg/dl and urea was 26 mg/dl. Complete blood counts, urine tests, liver and thyroid function tests of the patient were evaluated as within normal ranges. Serum uric acid level was 0.7 mg/dl and significant hypouricemia was continuing. Control of serum uric acid level was 0.11 mg/dl and a 24-hour urine uric acid level was measured as 345 mg/day, the fractional excretion of uric acid was calculated as 46 %. Causes of hypouricemia are given in table 1 and table 2 and detailed clinical
Mustafa ÇAKAR GATA, İç Hastalıkları AD., Ankara. E-posta:
[email protected] Makalenin gönderilme tarihi: 10.02.2010
Makalenin kabul edilme tarihi: 05.06.2012
Anatol J Clin Investig 2013;7(4):225-227
ÜNAL et al.
and laboratory examinations were appreciated as in accordance with familial renal hypouricemia. Table 1: Reasons of Hypouricemia Decreased Production -Hereditary xanthinuria -Liver diseases -Allopurinol treatment -Purine nucleoside phosphorylase deficiency Increased Renal Excretion -Familial renal hypouricemia -Fanconi syndrome -Intracranial disease -HIV -Pregnancy -Use of TPN -D.M. -Drugs
renal tubular transport defects such as Fanconi's syndrome. Low serum uric acid levels are often asymptomatic, while renal hypouricemia may be complicated by the formation of uric acid stones or acute renal failure. Acute renal failure following an exercise has been defined with an increasing proportion in patients with familial renal hypouricemia. 90% of cases were male and patients symptoms usually appeared after a heavy exercise. Symptoms, often nausea, vomiting and flank pain, begin within 6-12 hours. Although some of the patients with acute renal failure need for hemodialysis, all patients reached the normal serum creatinine levels finally [8-10].
Table 2: Drugs that increase the renal excretion of uric acid (6) -High-dose salicylates -Asetohexamide -Dicoumarol -Sulfinpyrazone -Trimethoprim-sulfamethoxazole -Estrogen preparations -Losartan -Iopanoik acid Phenylbutazone Klorprotiksen Probenecid Azauridin
Discussion Uric acid occurs as the end product of adenosine and guanosine-based purine metabolism. Uric acid in the body is of endogenous origin (the transformation of muscle cells, nucleic acids) or exogenous origin (food). Purine nucleotides are destroyed as a result of the separation of the components making up the nucleotide in an order. As uricase enzyme does not exist in the human organism, the end product of this destruction is uric acid. Uric acid is mainly excreted through the urinary tract and 1/3 of the excretion is by the gastrointestinal tract. 98 % of it is in the free sodium-urate form in plasma and is subject to glomerular filtration, less than 5 % is bound to plasma proteins. About 10% of total uric acid reaching the tubules by filtration is excreted in the urine and the remaining 90 % is reabsorbed here [7]. Renal excretion of uric acid may be increased by uricosuric drugs, total parenteral nutrition or by
The pathogenesis of acute renal failure associated with renal hypouricemia has not been fully understood. Uric acid is a strong antioxidant and especially prevents injury of free oxygen radicals against the proximal tubule. In these patients, uric acid pool is very small and the static intracellular uric acid concentration is low. Not only daily uric acid excretion but also the amount of uric acid mobilized in the proximal tubule cells is in the normal limits. Exercise increases the production of free oxygen radicals during the increase of blood flow to muscles leading to reduced renal blood flow. In patients with low intracellular concentration of uric acid, this phenomenon leads to severe vasoconstriction. Increased production of oxygen free radicals are demonstrated in ischemia-reperfusion models. Acute renal failure following a heavy exercise is described with ischemia-reperfusion model [1113]. A diagnosis of familial renal hypouricemia is made with decreased serum uric acid levels and increased fractional excretion of uric acid (> 10%). Acute renal failure developing after a strenuous exercise is a clinically important clue. SLC22A12 gene mutations responsible for the construction of URAT1 is used for diagnostic detection [14].
Our case is important to be the first case reported in Turkey. It is a rare and perhaps overlooked disease, and attention should be focused on prevention of a potential permanent kidney failure with supportive therapy.
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