Compensatory renal growth due to neonatal ureteral obstruction: implications for clinical studies

Abstract

In response to unilateral ureteral obstruction (UUO), the contralateral kidney undergoes compensatory renal growth, which is enhanced in early development. We investigated the renal growth response to UUO in the neonatal rat. Within 2 days of birth, animals were subjected to sham-operation, complete UUO, or variable partial UUO, and kidneys were harvested 3-60 days later. Contralateral kidney weight increased after only 7 days of complete UUO. Increase in contralateral kidney weight was not significant for partial UUO until 45 days, but kidney/body weight ratio increased after only 14 days of 0.3 mm partial UUO. The rate of contralateral renal growth increased with age and with increasing severity of UUO. In rats subjected to 45 days UUO, glomerular area was proportional to kidney/body weight ratio (r =0.61, p <0.01). We conclude that the rate of compensatory renal growth is dependent on the severity and duration of obstruction, and takes place at the single nephron level. The results suggest that biologic variability limits the early detection of compensatory renal growth, which is compounded by limitations in measuring renal size by clinical imaging. Factoring kidney length (or volume) by intervertebral length (or body surface area) should improve the precision of tracking renal growth.

Renal functional decline and glomerulotubular injury are arrested but not restored by release of unilateral ureteral obstruction (UUO)

“…Such growth of the contralateral kidney could result from a delayed response to temporary contralateral UUO, or a persistent stimulus due to decrease in GFR of the obstructed kidney. Unfortunately, little is known regarding the mechanisms that promote contralateral renal hypertrophy during UUO (22). Examination of the contralateral kidney after reversible UUO is of interest since it reflects adaptation to the recovery of the previously obstructed kidney.…”

The early and late period alterations on the contralateral renal parenchyma secondary to unilateral ureteropelvic junction obstruction: experimental study

“…Literatürde tam veya kısmi ÜPB tıkanıklığında biyokimyasal, ultrastrüktürel ve fonksiyonel parametreler açısından karşı taraf böbrekte oluşan yanıtı inceleyen birkaç çalışma (2,7,26,32,33) vardır. Bilindiği gibi ÜPB tı-kanıklığı karşı böbrekte kompansatuvar hipertrofiye neden olmaktadır.…”

“…Karşı böbrekte toplam nefron sayısı değişmeksizin, toplam DNA içeriğinin artmasına bağlı olarak ağırlık artışı görülür (26) . Görülen bu ağır-lık artışı tıkanıklığın şiddeti ve süresine bağlıdır (32) .…”

“…Bu histopatolojik değişikliklerden de renal kan akı-mının azalmasına yani iskemiye bağlı olarak üretimi artan bazı mediatörlerin ve serbest oksijen radikallerinin sorumlu olduğu gösterilmiştir (1,3,27,30) . Literatür-de tam veya kısmi ÜPB tıkanıklığında biyokimyasal, ultrastrüktürel ve fonksiyonel parametreler açısından karşı taraf böbrekte oluşan yanıtı inceleyen birkaç ça-lışma (2,7,26,32,33) vardır. Buna karşın literatürde yalnızca bir çalışmada (7) karşı böbrekte de etkilenen böbrek-te görülen histopatolojik değişiklikler ve apopitozis ortaya konmuştur.…”

Compensatory renal growth and mitochondrial function: the influence of warm ischemia and reperfusion

“…[7][8][9][10] The mechanisms responsible for CRG are not known with certainty, although a number of biochemical and molecular changes have been observed that could be involved such as several growth factors, interleukins and the rennin-angiotensin system. [11][12][13][14][15] The beginning of renal transplantation programs arouses a new opportunity for studying CRG in association with renal ischemia/reperfusion injury. Upon hypoxic injury, the depletion of ATP causes mitochondrial dysfunction, and accumulation of intracellular sodium, calcium and reactive oxygen species.…”