In-vivo techniques for determining nephron number

Denic, Aleksandar; Elsherbiny, Hisham E.; Rule, Andrew D.

doi:10.1097/mnh.0000000000000540

Cited by 20 publications

(14 citation statements)

References 50 publications

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“…Surrogates for nephron number have been investigated by many groups because functional nephron number cannot be directly measured in humans (49). Surrogates such as birth weight, kidney size, and biopsy findings have been evaluated and reviewed by several groups (49,50). However, surrogates for nephron number have had limited utility due the lack of large studies and challenges with validation.…”

Section: Discussionmentioning

confidence: 99%

Image analysis techniques to map pyramids, pyramid structure, glomerular distribution, and pathology in the intact human kidney from 3-D MRI

Charlton

Parvin

et al. 2021

American Journal of Physiology-Renal Physiology

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Kidney pathologies are often highly heterogenous. To comprehensively understand kidney structure and pathology, it is critical to develop tool to map tissue microstructure in the context of the whole, intact organ. Magnetic resonance imaging (MRI) can provide a unique, three-dimensional (3D) view of the kidney and allows for measurement of multiple pathologic features. Here, we develop a platform to systematically render and map gross and microstructural features of the human kidney based on 3D MRI. These features include pyramid number and morphology, and associated medulla and cortex. in a subset of these kidneys, we also map individual glomeruli and glomerular volumes using cationic ferritin enhance-MRI to report intra-renal heterogeneity in glomerular density and size. Finally, we render and measure regions of nephron loss due to pathology and individual glomerular volumes in each pyramidal unit. This work provides new tools to comprehensively evaluate the kidney across scales, with potential applications in anatomical and physiological research, transplant allograft evaluation, biomarker development, biopsy guidance, and therapeutic monitoring. These image rendering and analysis tools could eventually impact the field of transplantation medicine to improve longevity matching of donor allografts and recipients and reduce discard rates through the direct assessment of donor kidneys.

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Section: Discussionmentioning

confidence: 99%

Image analysis techniques to map pyramids, pyramid structure, glomerular distribution, and pathology in the intact human kidney from 3-D MRI

Charlton

Parvin

et al. 2021

American Journal of Physiology-Renal Physiology

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“…From animal and human studies, low nephron endowment at birth is a manifestation of CAKUT. To understand the prevalence of low nephron number, there is a need for methods to capture this phenotype in real time and not only from postmortem studies (52). Indirect approximations of nephron number have incorporated birth weight and estimates of nephron loss with age, but these formulas have not been validated in large populations with diverse ethnicities (53).…”

Section: Nephron Endowment and Congenital Anomalies Of The Kidneys And Urinary Tracts In The Futurementioning

confidence: 99%

A Primer on Congenital Anomalies of the Kidneys and Urinary Tracts (CAKUT)

Murugapoopathy¹,

Gupta²

2020

CJASN

109

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Congenital anomalies of the kidneys and urinary tracts (CAKUT) are disorders caused by defects in the development of the kidneys and their outflow tracts. The formation of the kidneys begins at week 3 and nephrogenesis continues until week 36, therefore, the kidneys and outflow tracts are susceptible to environmental risk factors that perturb development throughout gestation. Many genes have been implicated in kidney and outflow tract development, and mutations have been identified in patients with CAKUT. In severe cases of CAKUT, when the kidneys do not form, the fetus will not survive. However, in less severe cases, the baby can survive with combined kidney and outflow tract defects or they may only be identified in adulthood. In this review, we will cover the clinical presentation of CAKUT, its epidemiology, and its long-term outcomes. We will then discuss risk factors for CAKUT, including genetic and environmental contributions. Although severe CAKUT is rare, low nephron number is a much more common disorder with its effect on kidney function increasingly apparent as a person ages. Low nephron number appears to arise by the same mechanisms as CAKUT, but it differs in terms of the magnitude of the insult and the timing of when it occurs during gestation. By understanding the causes of CAKUT and low nephron number, we can begin to identify preventive treatments and establish clinical guidelines for how these patients should be followed.

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“…Each lost nephron increases the workload on the remnant nephrons accelerating also their demise, up to when nephron number is too low to avoid uraemia. Unfortunately, a marker of nephron number suitable for clinical practice is not yet available [6].…”

Section: P a T H O P H Y S I O L O G Y O F C K Dmentioning

confidence: 99%

SGLT2 inhibition requires reconsideration of fundamental paradigms in chronic kidney disease, ‘diabetic nephropathy’, IgA nephropathy and podocytopathies with FSGS lesions

Anders

Peired

Romagnani

2020

Nephrology Dialysis Transplantation

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In 2020, the Dapagliflozin and Prevention of Adverse Outcomes in Chronic Kidney Disease (DAPA-CKD) trial first demonstrated that inhibition of the sodium–glucose transporter-2 (SGLT2) with dapagliflozin attenuates the progression of chronic kidney disease (CKD) with proteinuria in patients with or without diabetes at an unprecedented effect size. These results have far-reaching implications for a series of traditional concepts in Nephrology. It now became obvious that CKD with and without diabetes involves a predominant SGLT2-driven pathophysiology compared with the other pathogenic pathways currently under consideration. As SGLT2 inhibition is similarly efficacious in diabetic and non-diabetic CKD with proteinuria, treating CKD rather than ‘diabetic nephropathy’ becomes the central paradigm. Indeed, in older adults with type 2 diabetes, CKD is rather of multifactorial origin. As the DAPA-CKD trial included more patients with immunoglobulin A nephropathy (IgAN) than any of the previous IgAN trials, dual renin-angiotensin/SGLT2 inhibition may become the new standard. The same applies for patients with podocytopathy-related focal segmental glomerulosclerosis lesions. From now on, IgAN and podocytopathy trials without SGLT2 inhibition as background therapy and without glomerular filtration rate decline as primary outcome criterion will be of limited value. These and other potential implications will trigger broad discussions and secondary research activities with conclusions difficult to predict today. However, one is for sure: Nephrology after the DAPA-CKD trial will be not the same as it was before. Finally!

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In-vivo techniques for determining nephron number

Cited by 20 publications

References 50 publications

Image analysis techniques to map pyramids, pyramid structure, glomerular distribution, and pathology in the intact human kidney from 3-D MRI

Image analysis techniques to map pyramids, pyramid structure, glomerular distribution, and pathology in the intact human kidney from 3-D MRI

A Primer on Congenital Anomalies of the Kidneys and Urinary Tracts (CAKUT)

SGLT2 inhibition requires reconsideration of fundamental paradigms in chronic kidney disease, ‘diabetic nephropathy’, IgA nephropathy and podocytopathies with FSGS lesions

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