The kidney vasculature is critical for renal function, but its developmental assembly mechanisms remain poorly understood and models for studying its assembly dynamics are limited. Here, we tested whether the embryonic kidney contains endothelial cells (ECs) that are heterogeneous with respect to VEGFR2/Flk1/KDR, CD31/PECAM, and CD146/MCAM markers. Tie1Cre;R26R(YFP)-based fate mapping with a time-lapse in embryonic kidney organ culture successfully depicted the dynamics of kidney vasculature development and the correlation of the process with the CD31(+) EC network. Depletion of Tie1(+) or CD31(+) ECs from embryonic kidneys, with either Tie1Cre-induced diphtheria toxin susceptibility or cell surface marker-based sorting in a novel dissociation and reaggregation technology, illustrated substantial EC network regeneration. Depletion of the CD146(+) cells abolished this EC regeneration. Fate mapping of green fluorescent protein (GFP)-marked CD146(+)/CD31(-) cells indicated that they became CD31(+) cells, which took part in EC structures with CD31(+) wild-type ECs. EC network development depends on VEGF signaling, and VEGF and erythropoietin are expressed in the embryonic kidney even in the absence of any external hypoxic stimulus. Thus, the ex vivo embryonic kidney culture models adopted here provided novel ways for targeting renal EC development and demonstrated that CD146(+) cells are critical for kidney vasculature development.
Ischemia-reperfusion injury (IRI) occurs when the blood supply to an organ is temporarily reduced and then restored. Kidney IRI is a form of acute kidney injury, which often progresses to kidney fibrosis. Necroptosis is a regulated necrosis pathway that has been implicated in kidney IRI.
The rare disease Familial Hyperkalemic Hypertension (FHHt) is caused by mutations in the genes encoding Cullin 3 (CUL3), Kelch-Like 3 (KLHL3), and two members of the With-No-Lysine [K] (WNK) kinase family, WNK1 and WNK4. In the kidney, these mutations ultimately cause hyperactivation of NCC along the renal distal convoluted tubule. Hypertension results from increased NaCl retention, and hyperkalemia by impaired K secretion by downstream nephron segments.
Renal artery thrombosis is an uncommon but serious cause of acute kidney injury that can result in permanent loss of function. It is frequently misdiagnosed due to its non-specific appearance, which can mimic renal colic and other more common causes of abdominal pain. There is no agreement on the first-line treatment and no prospective studies comparing thrombolysis, anticoagulation and embolectomy.
Deceased-donor kidney allografts are exposed to ischemic injury during ex vivo transport due to the lack of blood oxygen supply. Hypothermic machine perfusion (HMP) effectively reduces the risk of delayed graft function in kidney transplant recipients compared to standard cold storage. However, no free software implementation is available to analyze HMP data for state-of-the-art visualization and quality control.
Purpose Of Review: This review examines the effects of occupational heat stress on kidney health. It focuses on the role of hyperthermia in the development of acute kidney injury (AKI) and its potential progression to chronic kidney disease of nontraditional etiology (CKDnt). We highlight the physiological mechanisms by which hyperthermia affects kidney function and discuss emerging preventive strategies.
