Publication: Evre 2 ve evre 3 nondiyabetik kronik böbrek yetmezliği hastalarında serum ürik asit düzeyi ve hastalık progresyonu arasındaki ilişki
Abstract
GİRİŞ: Çeşitli nedenlere bağlı gelişen kronik böbrek yetmezliği genellikle son dönem böbrek yetmezliğine ilerler. Altta yatan neden sıklıkla tedavi edilemez. Deneysel çalışmalar kronik böbrek yetmezliğindeki progresyonun büyük ölçüde sekonder faktörler ile ilişkili olduğunu göstermektedir. Bu faktörler ise her zaman altta yatan hastalık ile ilişkili değildir. Hiperürisemi azalmış ürik asit eksresyonuna bağlı olarak kronik böbrek yetmezliği hastalarında gelişen bir durumdur ve hiperüriseminin kronik böbrek hastalığı progresyonu hızlandırdığı öne sürülse de konuyla ilgili çalışmaların sonuçları çelişkilidir. Biz de bu retrospektif çalışmada evre 3 ve 4 diabetik olmayan KBY hastalarında serum ürik asit düzeyi ile KBY progresyonu arasındaki ilişkiyi araştırdık. GEREÇ-YÖNTEM: Nefroloji polikliniğimizde en az bir yıldır takip edilen 30 yaş üzeri ve 90 yaş altındaki evre 3 ve 4 diabetik olmayan KBY hastalarının dosya kayıtlarından ilk başvurularında bakılan serum ürik asit düzeyleri bazal ürik asit değerleri olarak kaydedildi. Hastaların BUN, kreatinin ve MDRD formülü ile hesaplanan eGFR değerleri yıllık olarak kaydedildi. Hastaların kontrollerde bakılan serum ürik asit düzeyleri yıllık ortalama değerler olarak kaydedildi. Hastaların ilk başvurularındaki boy, kilo, yaş, cinsiyet, BMI, sigara kullanımı, kan basıncı, ESBACH, albuminüri değerleri ve allopurinol, ACE inhibitörü, ARB, losartan, KKB, tiazid ve furosemid kullanım durumları kaydedildi. SONUÇ: Erkeklerde yıllık GFR azalması (3.8±4.7 ml/ dk) kadınlara göre (1.7±2.3 ml/ dk) anlamlı olarak daha yüksek saptandı (p<0.032). Çok değişkenli lineer regresyon analizinde sadece başlangıç serum albümin, başlangıç eGFR ve 1 yıllık ürik asit ortalaması GFR’ deki ortalama yıllık azalma hızı ile ilişkili bulundu. Başlangıçta hiperürisemisi olan 49 hastada hiperürisemisi olmayan 22 hastaya göre ortalama yıllık GFR azalması açısından anlamlı fark saptanmadı sırasıyla (2.9±4.5 ml/ dk karşın 2.0±2.71, p=0.894). Allopurinol kullanan grupta kullanmayanlar arasında ortalama yıllık GFR azalması benzer saptandı (sırasıyla 2.2±2.4 ml/ dk karşın 3.2±4.3 ml/ dk,p=0.323). TARTIŞMA: KBY erken evrelerinde dahi hiperürisemi sık rastlanan bir durumdur. Ancak ürik asit ile GFR düşüşü arasındaki nedensellik ilişkisi üzerine yapılan çalışmaların sonuçları çelişkilidir. Benzer dizayna sahip çalışmaların sonuçları ile uyumlu olarak biz de çalışmamızın sonucunda başlangıç serum ürik asit düzeyi ile yıllık ortalama GFR azalması arasında anlamlı bir ilişki saptamadık. Bu da hiperüriseminin kronik böbrek hastalığı progresyonunu hızlandıran bir neden olmaktan ziyade GFR’ deki azalmanın bir sonucu olduğu görüşünü desteklemektedir.
INTRODUCTION: Variety of Chronic Kidney Disease (CKD) usually progress to End Stage Renal Disease (ESRD). The underlying etiology often cannot be treated. Experimental studies suggest that progression in CKD largely due to secondary factor. These factors are not always related to the underlying disease. Hyperuricemia is a common situation in CKD patients. Some studies suggest that hyperuricemia accelerate the progression to ESRD, but the results are still contradictory. In this retrospective study we aimed to investigate the relationship between serum uric acid and CKD progression in stage 3 and 4 non-diabetic CKD patients. MATERIALS AND METHODS: The study group was stage 3 and 4 non-diabetic CKD patients between 30-90 years old and followed more than a year in our nephrology policlinic. The serum uric acid level recorded when the patient has first applied to our outpatient clinic has been taken in to account as uric acid baseline. eGFR (which have been calculated using MDRD), BUN and creatinin values have been recorded annually. The latter records of serum uric acid level has been recorded as annual average values. Age, gender, BMI, blood pressure, ESBACH, albuminurea values and use of allopurinol, ACE inhibitor, ARB, losartan, calcium canal blokers, thiazide diuretics, furosemid have been recorded as stated in the file from the first application of the patient. The usage of allopurinol during follow up was also recorded. RESULTS: Annual reduction of GFR in male patients (3.8+-4.7ml/ dk) have been determined significantly higher than the reduction in female patients(1.7+-2.3 ml/ dk) (p<0.032). In multivariate linear regression analysis, only variables related with the reduction in annual GFR were baseline serum albumin, baseline eGFR, annual average of uric acid. When compared the group without hyperuricemia (n:22), hyperuricemic patient’s (n:49) annual GFR reduction was not significantly higher (respectively 2.9+-4.5 ml/ dk comparing to 2.0+-2.71 ml/ dk, p=0.894). The group using allopurinol and the other group not using allopurinol were similar when we consider the reduction in annual GFR (respectively 2.2+-2.4 ml/ dk comparing to 3.2+-4.3 ml/ dk, p=0.323). DISCUSSION: Even in the early stages of CKD hyperuricemia is a common situation. Even though the result of the studies made to find out the relationship between the reduction of GFR and uric acid is contradictory. Parallel to the other studies made in similar design we couldn’t find any reasonable relationship between the reduction of uric acid and GFR. Thus this finding supports that hyperuricemia is a result of the reduction in GFR, rather than being a reason of accelerating progression in CKD.
INTRODUCTION: Variety of Chronic Kidney Disease (CKD) usually progress to End Stage Renal Disease (ESRD). The underlying etiology often cannot be treated. Experimental studies suggest that progression in CKD largely due to secondary factor. These factors are not always related to the underlying disease. Hyperuricemia is a common situation in CKD patients. Some studies suggest that hyperuricemia accelerate the progression to ESRD, but the results are still contradictory. In this retrospective study we aimed to investigate the relationship between serum uric acid and CKD progression in stage 3 and 4 non-diabetic CKD patients. MATERIALS AND METHODS: The study group was stage 3 and 4 non-diabetic CKD patients between 30-90 years old and followed more than a year in our nephrology policlinic. The serum uric acid level recorded when the patient has first applied to our outpatient clinic has been taken in to account as uric acid baseline. eGFR (which have been calculated using MDRD), BUN and creatinin values have been recorded annually. The latter records of serum uric acid level has been recorded as annual average values. Age, gender, BMI, blood pressure, ESBACH, albuminurea values and use of allopurinol, ACE inhibitor, ARB, losartan, calcium canal blokers, thiazide diuretics, furosemid have been recorded as stated in the file from the first application of the patient. The usage of allopurinol during follow up was also recorded. RESULTS: Annual reduction of GFR in male patients (3.8+-4.7ml/ dk) have been determined significantly higher than the reduction in female patients(1.7+-2.3 ml/ dk) (p<0.032). In multivariate linear regression analysis, only variables related with the reduction in annual GFR were baseline serum albumin, baseline eGFR, annual average of uric acid. When compared the group without hyperuricemia (n:22), hyperuricemic patient’s (n:49) annual GFR reduction was not significantly higher (respectively 2.9+-4.5 ml/ dk comparing to 2.0+-2.71 ml/ dk, p=0.894). The group using allopurinol and the other group not using allopurinol were similar when we consider the reduction in annual GFR (respectively 2.2+-2.4 ml/ dk comparing to 3.2+-4.3 ml/ dk, p=0.323). DISCUSSION: Even in the early stages of CKD hyperuricemia is a common situation. Even though the result of the studies made to find out the relationship between the reduction of GFR and uric acid is contradictory. Parallel to the other studies made in similar design we couldn’t find any reasonable relationship between the reduction of uric acid and GFR. Thus this finding supports that hyperuricemia is a result of the reduction in GFR, rather than being a reason of accelerating progression in CKD.