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      Solitary Functioning Kidney in Children - A Follow-Up Study

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          Background/Aims: This study aims to assess the cumulative incidence of elevated albuminuria, hypertension and decreased estimated glomerular filtration rate (eGFR) to identify possible renal injury in children with SFK. Methods: Forty-two children with SFK (23 boys; 27 congenital) were included in a prospective follow-up study. Blood pressure, albuminuria and eGFR were assessed repeatedly and the cumulative incidence rate of various forms of renal injury, overall and by type of etiology, were evaluated. Finally, renal injury-free survival was analyzed. Results: Mean follow-up was until age 11.3 years (SD 6.3 years). During follow-up, 16 (38.1%) patients met the criteria for renal injury, defined as hypertension (10; 23.8%), severely increased albuminuria (3; 7.1%) and a significantly impaired eGFR (<60ml/min/1.73m<sup>2</sup>) (5; 11.9%) and/or use of antihypertensive or antiproteinuric medication (11; 26.2%). Children with CAKUT in SFK had a significantly higher incidence of renal injury. The median time to develop renal injury was 12.8 years. Conclusion: A substantial proportion of children with SFK develop renal injury during childhood, especially those with CAKUT in the SFK. Therefore, close follow-up of albuminuria, blood pressure and eGFR are warranted to identify chronic kidney disease in its early stages.

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          Nephron number in patients with primary hypertension.

          A diminished number of nephrons has been proposed as one of the factors contributing to the development of primary hypertension. To test this hypothesis, we used a three-dimensional stereologic method to compare the number and volume of glomeruli in 10 middle-aged white patients (age range, 35 to 59 years) with a history of primary hypertension or left ventricular hypertrophy (or both) and renal arteriolar lesions with the number and volume in 10 normotensive subjects matched for sex, age, height, and weight. All 20 subjects had died in accidents. Patients with hypertension had significantly fewer glomeruli per kidney than matched normotensive controls (median, 702,379 vs. 1,429,200). Patients with hypertension also had a significantly greater glomerular volume than did the controls (median, 6.50x10(-3) mm3 vs. 2.79x10(-3) mm3; P<0.001) but very few obsolescent glomeruli. The data support the hypothesis that the number of nephrons is reduced in white patients with primary hypertension. Copyright 2003 Massachusetts Medical Society
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            Glomerular number and size in autopsy kidneys: the relationship to birth weight.

            In the Southeast United States, African Americans have an estimated incidence of hypertension and end-stage renal disease (ESRD) that is five times greater than Caucasians. Higher rates of low birth weight (LBW) among African Americans is suggested to predispose African Americans to the higher risk, possibly by reducing the number of glomeruli that develop in the kidney. This study investigates the relationships between age, race, gender, total glomerular number (Nglom), mean glomerular volume (Vglom), body surface area (BSA), and birth weight. Stereologic estimates of Nglom and Vglom were obtained using the physical disector/fractionator combination for autopsy kidneys from 37 African Americans and 19 Caucasians. Nglom was normally distributed and ranged from 227,327 to 1,825,380, an 8.0-fold difference. A direct linear relationship was observed between Nglom and birth weight (r = 0.423, P = 0.0012) with a regression coefficient that predicted an increase of 257,426 glomeruli per kilogram increase in birth weight (alpha = 0.050:0.908). Among adults there was a 4.9-fold range in Vglom, and in adults, Vglom was strongly and inversely correlated with Nglom (r =-0.640, P = 0.000002). Adult Vglom showed no significant correlation with BSA for males (r = -0.0150, P = 0.936), although it did for females (r = 0.606, P = 0.022). No racial differences in average Nglom or Vglom were observed. Birth weight is a strong determinant of Nglom and thereby of glomerular size in the postnatal kidney. The findings support the hypothesis that LBW by impairing nephron development is a risk factor for hypertension and ESRD in adulthood.
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              Human nephron number: implications for health and disease.

              Several studies have shown that total nephron (glomerular) number varies widely in normal human kidneys. Whereas the studies agree that average nephron number is approximately 900,000 to 1 million per kidney, numbers for individual kidneys range from approximately 200,000 to >2.5 million. Several studies have shown loss of glomeruli due to age-related glomerulosclerosis. The rates of loss vary among individuals depending upon blood pressure, diseases affecting the kidney, and other attributes of health, but most of the variation in nephron number is present at birth and is therefore developmentally determined. For example, in a relatively small study of nephron number in 15 children <3 months of age, we found that nephron number ranged from approximately 250,000 to 1.1 million. Given that no new nephrons are formed in human kidneys after approximately 36 weeks' gestation, much interest has focused on renal function and health in individuals born with relatively low nephron endowment. Several studies have reported a direct correlation between birth weight and nephron number and an indirect association between nephron number and blood pressure. Associations between low birth weight and cardiovascular disease, including hypertension, have also been widely reported. This report provides an update on our current knowledge of human nephron number and the associations with adult health and disease.

                Author and article information

                Kidney Blood Press Res
                Kidney and Blood Pressure Research
                S. Karger AG
                November 2014
                09 August 2014
                : 39
                : 4
                : 272-278
                aPaediatric Department, Faculty of Medicine, Safarik University; bGraduate School Kosice Institute for Society and Health, Safarik University, Kosice, Slovak Republic; cUniversity of Groningen, University Medical Center Groningen, Department of Community &amp; Occupational Health, Groningen, The Netherlands
                Author notes
                *Gabriel Kolvek, MD, Paediatric Department, Faculty of Medicine, Safarik University, Tr. SNP 1,, 040 11 Kosice (Slovak Republic), E-Mail
                355804 Kidney Blood Press Res 2014;39:272-278
                © 2014 S. Karger AG, Basel

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                Pages: 7
                Original Paper


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