A Comparative Study of Size and Function of the Remnant Kidney in Patients Nephrectomized in Childhood for Wilms’Tumor and Hydronephrosis

Wikstad, I.; Pettersson, B.; Elinder, Göran; Sökücü, Semra; Aperia, Anita

doi:10.1111/j.1651-2227.1986.tb10222.x

Cited by 54 publications

(19 citation statements)

References 26 publications

(2 reference statements)

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“…[23][24][25] Despite these studies, the long-term outlook for developing hypertension, proteinuria, and renal failure still remains somewhat controversial. Studies that have evaluated children who have had nephrectomy 21,26,27 or adults that served as a kidney donor 28,29 have found little or no difference in renal function and/or injury compared with control subjects. However, several recent studies have found kidney donors are at an increased risk (up to 8-fold) to develop renal failure.…”

Section: Discussionmentioning

confidence: 99%

Nephron Deficiency and Predisposition to Renal Injury in a Novel One-Kidney Genetic Model

Wang¹,

Johnson²,

White³

et al. 2015

Journal of the American Society of Nephrology

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Some studies have reported up to 40% of patients born with a single kidney develop hypertension, proteinuria, and in some cases renal failure. The increased susceptibility to renal injury may be due, in part, to reduced nephron numbers. Notably, children who undergo nephrectomy or adults who serve as kidney donors exhibit little difference in renal function compared with persons who have two kidneys. However, the difference in risk between being born with a single kidney versus being born with two kidneys and then undergoing nephrectomy are unclear. Animal models used previously to investigate this question are not ideal because they require invasive methods to model congenital solitary kidney. In this study, we describe a new genetic animal model, the heterogeneous stock-derived model of unilateral renal agenesis (HSRA) rat, which demonstrates 50%-75% spontaneous incidence of a single kidney. The HSRA model is characterized by reduced nephron number (more than would be expected by loss of one kidney), early kidney/glomerular hypertrophy, and progressive renal injury, which culminates in reduced renal function. Long-term studies of temporal relationships among BP, renal hemodynamics, and renal function demonstrate that spontaneous single-kidney HSRA rats are more likely than uninephrectomized normal littermates to exhibit renal impairment because of the combination of reduced nephron numbers and prolonged exposure to renal compensatory mechanisms (i.e., hyperfiltration). Future studies with this novel animal model may provide additional insight into the genetic contributions to kidney development and agenesis and the factors influencing susceptibility to renal injury in individuals with congenital solitary kidney.

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Section: Discussionmentioning

confidence: 99%

Nephron Deficiency and Predisposition to Renal Injury in a Novel One-Kidney Genetic Model

Wang¹,

Johnson²,

White³

et al. 2015

Journal of the American Society of Nephrology

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“…Renal size (measured by ultrasound) was evaluated using the formula: length6width6(longitudinal+transverse depth)/ 260.523 (Wikstad et al, 1986).…”

Section: Renal Investigationsmentioning

confidence: 99%

“…Reported effects after treatment for Wilms' tumour have included reduction in glomerular filtration rate (GFR) (Walker et al, 1982;Robitalle et al, 1985;Levitt et al, 1992), microalbuminuria (Levitt et al, 1992;di Tullio et al, 1996) (rarely resulting in hyperfiltration induced glomerulosclerosis and subsequent renal failure), failure of compensatory hypertrophy of the remaining kidney (Wikstad et al, 1986;Makipernaa et al, 1991;Levitt et al, 1992) and hypertension (Levitt et al, 1992).…”

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confidence: 99%

Nephrotoxicity in survivors of Wilms' tumours in the North of England

et al. 2002

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One aspect of concern for survivors of Wilms' tumour has been the late outcome in terms of renal function. Previous studies have documented low glomerular filtration rate and high blood pressure in some patients. Furthermore, disorders in tubular function (especially urinary concentration defects) have been suggested but not confirmed in small studies. The aim of this study was to determine the prevalence and nature of subclinical and overt glomerular, proximal and distal renal tubular toxicity in a population based cohort of survivors of Wilms' tumour. Forty patients (24 female) with a median age of 4.3 years (3 months -11.8 years) at diagnosis were studied. Median follow-up was 8.8 (range 0.06 -27.5) years. Glomerular filtration rate was measured by 51 Cr-EDTA plasma clearance, proximal tubular function by electrolyte fractional excretions, urine excretion of low molecular weight proteins (retinol-binding protein) and renal tubular enzymes (alanine aminopeptidase; Nacetylglucosaminidase) and distal tubular function by the osmolality of the first two urines of the day on 3 consecutive days. Renal size (ultrasound) and blood pressure were also measured. Mean (range) glomerular filtration rate was 100 (61 -150) ml min 71 1.73 m 72 . Nine were below the reference range for healthy individuals with two kidneys. Most serum electrolyte concentrations (sodium, potassium, chloride, calcium, magnesium and phosphate) fell within the normal range for age, as did the fractional excretions. The values that fell outside the normal range were only marginally abnormal. Subclinical measures of tubular toxicity (retinal-binding protein, alanine aminopeptidase, N-acetylglucosaminidase) were abnormal in only four patients. Thirty-seven patients achieved maximal urine osmolalities 5800 mOsm kg 71 , but three failed to achieve this value even after DDAVP administration. Two patients had evidence of increased urinary albumin excretion. Compensatory renal hypertrophy was seen in all but two patients, but blood pressure was within normal limits in all patients. Current and past treatment for Wilms' tumour does not have any clinically important nephrotoxic effect in the majority of patients. This finding will enable paediatric oncologists to reassure patients and parents that treatment for Wilms' tumour rarely causes long-term renal impairment.

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“…Several studies have shown that there is compensatory renal growth in patients treated for Wilms' tumour with multimodality therapy (Walker et al, 1982;Luttenegger et al, 1975;Dinkel et al, 1988), but less than in children who have nephrectomy for non-malignant conditions. There are few reports of both renal growth and function in long-term survivors of Wilms' tumour and the number of patients in these studies is small (Wikstad et al, 1986;Makipernaa et al, 1991).…”

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confidence: 99%