Association of low birth weight and prematurity with clinical outcomes of childhood nephrotic syndrome: a prospective cohort study

Konstantelos, Natalia; Banh, Tonny; Patel, Vaidehi; Vasilevska-Ristovska, Jovanka; Borges, Karlota; Hussain-Shamsy, Neesha; Noone, Damien; Hébert, Diane; Radhakrishnan, Seetha; Licht, Christoph; Langlois, Valérie S.; Pearl, Rachel; Parekh, Rulan S.

doi:10.1007/s00467-019-04255-1

Cited by 13 publications

(12 citation statements)

References 35 publications

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“…12 As in other diseases, weight at birth, which is associated with total number of nephrons, may influence the clinical phenotype of MCD. [31][32][33][34] In the current study, mean SNGFR and SNUPE values in the low-nephron group were approximately 3.0-and 3.4-fold those in the high-nephron group, respectively, although mean eGFR, CL cr , and UPE per body values of the low-nephron group were comparable to those of the high-nephron group. By contrast, there were no significant differences in body mass index or blood pressure between the subgroups, which could influence SNGFR and SNUPE.…”

Section: Discussioncontrasting

confidence: 52%

“…Previous studies indicated that low birth weight, an important explanatory factor for low nephron number, is associated with an increased incidence and relapse of steroid-sensitive MCD in children. 33,34 Considering that MCD is an immunologic disease frequently triggered by infections, changes in postinfectious response associated with low birth weight may influence kidney disease outcomes, as suggested in a previous cohort study of Australian Aborigines. 44 This study had several important limitations.…”

Section: Discussionmentioning

confidence: 99%

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Nephron Number and Time to Remission in Steroid-Sensitive Minimal Change Disease

et al. 2020

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Rationale & Objective The response to corticosteroid therapy may differ among patients with minimal change disease (MCD). Previous studies have suggested that glomerular hypertrophy or low areal glomerular density in biopsy specimens, which may be related to fewer nephrons, is associated with such a difference. We examined the associations between nephron number and the therapeutic response to corticosteroids in patients with MCD. Study Design Retrospective cohort study. Setting & Participants 75 adult patients with a histologic diagnosis of MCD. Exposure Nephron number per kidney estimated based on the combination of unenhanced computed tomography and nonsclerotic volumetric glomerular density in kidney biopsy specimens. Outcomes Complete remission and relapse following corticosteroid therapy. Analytical Approach Multivariable Cox proportional hazard analyses of associations between factors, including nephron number, and outcomes. Results Mean age of patients was 45.9 years and 60.0% were men. Patients had an estimated glomerular filtration rate of 64.6 mL/min/1.73 m 2 and proteinuria of 8.7 g/d. The estimated total number of nonsclerotic glomeruli ranged from 1.07 to 18.77 ×10 5 per kidney among all patients. There were no significant differences in total amounts or selectivity of urinary protein excretion at biopsy among the tertile groups categorized by nephron number. All patients responded to corticosteroid therapy, but those with fewer nephrons had a delayed achievement of complete remission. Multivariable Cox proportional hazard analyses identified nephron number as a significant independent explanatory variable for the achievement of complete remission, with a hazard ratio of 1.10 (95% CI, 1.02-1.19)/100,000 nephrons per kidney. Nephron number in these patients was not associated with achievement of partial remission or relapse following complete remission. Limitation Retrospective design and sampling bias of needle biopsy. Conclusions A small nephron number in patients with MCD is associated with longer time to complete remission.

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Section: Discussioncontrasting

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Nephron Number and Time to Remission in Steroid-Sensitive Minimal Change Disease

et al. 2020

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“…Though there is no data on the quantity of the podocytes per glomerulus, there is evidence of reduced podocyte maturation and podocyte damage after IUGR [ 51 , 52 ]. Moreover, IUGR negatively influences the course of NS [ 53 , 54 ]. More recently, research has been conducted correlating prematurity and perinatal stress with glomerular vasculogenesis and postnatal glomerular damage.…”

Section: Discussionmentioning

confidence: 99%

“…In human cohort studies of patients with nephrotic syndrome, IUGR and prematurity have been found to be a risk factor for the development and aggravated course of nephrotic syndrome (NS). Several studies have shown that LBW and IUGR are associated with a steroid-dependent and steroid-resistant course of nephrotic syndrome [ 53 , 54 ]. Compared with normal birth weight, patients with LBW more often require immunosuppressive agents, have more relapses, and require a higher cumulative dose of steroids [ 55 ].…”

Section: Podocytopathymentioning

confidence: 99%

Prematurity, perinatal inflammatory stress, and the predisposition to develop chronic kidney disease beyond oligonephropathy

et al. 2020

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Prematurity and perinatal stress, such as intrauterine growth restriction (IUGR) and chorioamnionitis, are pathological processes creating an impaired intrauterine environment. These intrauterine factors are associated with the development of proteinuria, hypertension, and chronic kidney disease (CKD) later in life. Initially, this was thought to be secondary to oligonephropathy, subsequent glomerular hypertrophy, and hyperfiltration, leading to glomerulosclerosis, a further decrease in nephron number, and finally CKD. Nowadays, there is increasing evidence that prematurity and perinatal stress affect not only nephron endowment but also the maturation of podocytes and vasculogenesis. IUGR is associated with podocyte damage and an aggravated course of nephrotic syndrome. Moreover, preterm birth and IUGR are known to cause upregulation of the postnatal reninangiotensin system, resulting in hypertension. Chorioamnionitis causes damage to the glomeruli, thereby predisposing to the development of glomerulosclerosis. This review aims to summarize current knowledge on the influence of prematurity, IUGR, and chorioamnionitis on the development of different glomerular structures. After summarizing human and experimental data on low nephron number in general, a specific focus on the current understanding of podocyte and glomerular capillary formation in relation to prematurity and different causes of perinatal stress is presented.

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“…Individuals born preterm are at increased risk of chronic kidney disease (CKD) and kidney failure and have higher albumin excretion rates [ 5–8 ]. Most studies on long-term kidney function in preterm children and adults do not report a significant impact on blood creatinine or estimated or measured glomerular filtration rate (eGFR or mGFR) [ 9–11 ]. Kidney histological studies have suggested that preterm neonates show signs of single-nephron glomerular hyperfiltration [ 12 ], and authors have reported a higher eGFR or mGFR per unit of kidney volume in their cohorts of preterm children [ 13 ] or adults [ 11 ], suggestive of the single-nephron glomerular hyperfiltration.…”

Section: Introductionmentioning

confidence: 99%

Plasma copeptin is increased and associated with smaller kidney volume in young adults born very preterm

Flahault

Bollée

El-Jalbout

et al. 2021

Clinical Kidney Journal

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Background Plasma copeptin, a surrogate marker for vasopressin levels, is increased in neonates born preterm, particularly in those with a more severe neonatal course, as reflected by bronchopulmonary dysplasia. Copeptin levels in adulthood are unknown. Objective We aimed to determine whether plasma copeptin is higher in adults born preterm and associated with glomerular hyperfiltration. Methods In this case-control study of 101 adults born very preterm (<30 weeks of gestation) and 105 control adults born full-term, comprehensive clinical and biological assessment was performed, including blood pressure measurements, kidney ultrasound, and determination of plasma copeptin, renin activity, angiotensin II, aldosterone, apelin, sodium and potassium, serum and morning urine osmolality. Results Median (interquartile range, IQR) age in the study was 23.1 (21.2, 24.8) years, and 57% were females. In males, median (IQR) copeptin levels were 8.2 (6.3, 12.4) and 6.1 (4.3, 9.0) pmol/l in the preterm and the term groups, respectively (p = 0.022). In females, median (IQR) copeptin levels were 5.2 (3.9, 7.6) and 4.0 (2.8, 5.7) pmol/l in the preterm and the term groups, respectively (p = 0.005). Adults born preterm with history of bronchopulmonary dysplasia had further increased in copeptin levels. Kidney volume, adjusted to height, was smaller and albuminuria was higher in the preterm group, and both were associated with higher plasma copeptin levels. Conclusions Plasma copeptin is higher in young adults born preterm and is related to a more severe neonatal course and smaller kidney volume.

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Association of low birth weight and prematurity with clinical outcomes of childhood nephrotic syndrome: a prospective cohort study

Cited by 13 publications

References 35 publications

Nephron Number and Time to Remission in Steroid-Sensitive Minimal Change Disease

Nephron Number and Time to Remission in Steroid-Sensitive Minimal Change Disease

Prematurity, perinatal inflammatory stress, and the predisposition to develop chronic kidney disease beyond oligonephropathy

Plasma copeptin is increased and associated with smaller kidney volume in young adults born very preterm

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