Renal concentrating capacity as a marker for glomerular filtration rate

Nieto, Víctor Manuel García; Yanes, María I. Luis; Zamorano, Margarita Monge; González, María José; Aros, Carolina Peralta; Garin, Eduardo H.

doi:10.1111/j.1651-2227.2007.00587.x

Cited by 19 publications

(8 citation statements)

References 23 publications

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“…A recent study with 160 children with different renal diseases found a significant association between the inability to concentrate urine and glomerular filtration rate [36], but we did not found this in our cohort, since all patients had urinary concentration defect and the majority of them had normal GFR. The urinary concentration deficit in SCD is associated with red blood cells sickling and sickle cell crisis, with a possible reversion being described with repeated blood transfusions [37].…”

Section: Discussioncontrasting

confidence: 52%

Renal Tubular Dysfunction in Sickle Cell Disease

Silva

Vieira

Couto

et al. 2013

Kidney Blood Press Res

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Background/Aims: Kidney abnormalities are one of the main chronic complications of sickle cell disease (SCD). The aim of this study is to investigate the occurrence of renal tubular abnormalities among patients with SCD. Methods: This is a prospective study with 26 SCD adult patients in Brazil. Urinary acidification and concentration tests were performed using calcium chloride (CaCl₂), after a 12h period of water and food deprivation. Fractional excretion of sodium (FE_Na), transtubular potassium gradient (TTKG) and solute free water reabsorption (TcH₂O) were calculated. The SCD group was compared to a group of 15 healthy volunteers (control group). Results: Patient`s average age and gender were similar to controls. Urinary acidification deficit was found in 10 SCD patients (38.4%), who presented urinary pH >5.3 after CaCl₂ test. Urinary osmolality was significantly lower in SCD patients (355±60 vs. 818±202mOsm/kg, p=0.0001, after 12h period water deprivation). Urinary concentration deficit was found in all SCD patients (100%). FE_Na was higher among SCD patients (0.75±0.3 vs. 0.55±0.2%, p=0.02). The TTKG was higher in SCD patients (5.5±2.5 vs. 3.0±1.5, p=0.001), and TcH₂O was lower (0.22±0.3 vs. 1.1±0.3L/day, p=0.0001). Conclusions: SCD is associated with important kidney dysfunction. The main abnormalities found were urinary concentrating and incomplete distal acidification defect. There was also an increase in the potassium transport and decrease in water reabsorption, evidencing the occurrence of distal tubular dysfunction.

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Section: Discussioncontrasting

confidence: 52%

Renal Tubular Dysfunction in Sickle Cell Disease

Silva

Vieira

Couto

et al. 2013

Kidney Blood Press Res

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“…Alternatively, in subjects with lower GFR, the medullary urea gradient will be impaired because of a loss of functioning nephrons and interstitial fibrosis. Subjects with impaired GFR therefore have lower urinary osmolarity and higher urinary volume than subjects with normal renal function (49,50). Consequently, fluid reabsorption will be more difficult and higher VP levels will be necessary to maintain fluid balance.…”

Section: Discussionmentioning

confidence: 99%

Copeptin, a Surrogate Marker of Vasopressin, Is Associated with Disease Severity in Autosomal Dominant Polycystic Kidney Disease

Meijer¹,

Bakker²,

Jagt³

et al. 2011

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Experimental studies suggest a detrimental role for vasopressin in the pathogenesis of autosomal dominant polycystic kidney disease (ADPKD). However, it is unknown whether endogenous vasopressin concentration is associated with disease severity in patients with ADPKD.Design, setting, participants, & measurements Plasma copeptin concentration (a marker of endogenous vasopressin levels) was measured in 102 ADPKD patients (diagnosis based on Ravine criteria) by an immunoassay. Plasma and urinary osmolarity were also measured. To assess disease severity, GFR and effective renal blood flow were measured by continuous infusion of 125 I-iothalamate and 131 I-hippuran, total renal volume by magnetic resonance imaging, and 24-hour urinary albumin excretion by nephelometry. ResultsIn these ADPKD patients, copeptin was associated with the various markers of disease severity in ADPKD (positively with total renal volume [R ϭ 0.47] and albuminuria [R ϭ 0.39] and negatively with GFR [R ϭ Ϫ0.58] and effective renal blood flow [R ϭ Ϫ0.52], all P Ͻ 0.001). These associations were independent of age, gender, and use of diuretics. Copeptin was furthermore associated with plasma osmolarity (P Ͻ 0.001) but not with 24-hour urinary volume, 24-hour urinary osmolarity or fractional urea excretion (P ϭ 0.7, 0.9, and 0.3, respectively). ConclusionsOn cross-sectional analysis, copeptin is associated with disease severity in ADPKD patients, supporting the results of experimental studies that suggest that vasopressin antagonists have a renoprotective effect in ADPKD and offering a good prospect for clinical studies with these agents.

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“…All filtration units of the nephron drain through the collecting ducts of the papillary lobe(s), which are responsible for the final control of water excretion and therefore the urine concentration. In children, a reduced urine concentrating capacity is strongly associated with reduced glomerular filtration rate and tubular function (Nieto et al . 2008).…”

Section: Introductionmentioning

confidence: 99%

Prolonged prenatal hypoxia selectively disrupts collecting duct patterning and postnatal function in male mouse offspring

Walton

Singh

Little

et al. 2018

The Journal of Physiology

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Prenatal hypoxia is a common perturbation to arise during pregnancy, and can lead to adverse health outcomes in later life. The long-lasting impact of prenatal hypoxia on postnatal kidney development and maturation of the renal tubules, particularly the collecting duct system, is relatively unknown. In the present study, we used a model of moderate chronic maternal hypoxia throughout late gestation (12% O exposure from embryonic day 14.5 until birth). Histological analyses revealed marked changes in the tubular architecture of male hypoxia-exposed neonates as early as postnatal day 7, with disrupted medullary development and altered expression of Ctnnb1 and Crabp2 (encoding a retinoic acid binding protein). Kidneys of the RARElacZ line offspring exposed to hypoxia showed reduced β-galactosidase activity, indicating reduced retinoic acid-directed transcriptional activation. Wild-type male mice exposed to hypoxia had an early decline in urine concentrating capacity, evident at 4 months of age. At 12 months of age, hypoxia-exposed male mice displayed a compromised response to a water deprivation challenge, which was was correlated with an altered cellular composition of the collecting duct and diminished expression of aquaporin 2. There were no differences in the tubular structures or urine concentrating capacity between the control and hypoxia-exposed female offspring at any age. The findings of the present study suggest that prenatal hypoxia selectively disrupts collecting duct patterning through altered Wnt/β-catenin and retinoic acid signalling and this results in impaired function in male mouse offspring in later life.

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Renal concentrating capacity as a marker for glomerular filtration rate

Cited by 19 publications

References 23 publications

Renal Tubular Dysfunction in Sickle Cell Disease

Renal Tubular Dysfunction in Sickle Cell Disease

Copeptin, a Surrogate Marker of Vasopressin, Is Associated with Disease Severity in Autosomal Dominant Polycystic Kidney Disease

Prolonged prenatal hypoxia selectively disrupts collecting duct patterning and postnatal function in male mouse offspring

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