Kidney ischemia

More complications happen when failure of the kidney functions result in toxicity in various parts of the body which may cause septic shock, hypovolemia, and a need for surgery.

More emerging treatments are in the clinical trials such as Bendavia in targeting mitochondrial dysfunction and using Mesenchymal Stem Cell Therapy.

Several receptors agonists and antagonists have shown promise in animal studies; however, they have not been proven clinically yet.

[8] This is because in a high-fat diet model, accumulation of phospholipids resulted in enlarged lysosomes within proximal tubular cells.

Arteriosclerosis is defined as the thickening or stiffening or both of the blood vessels; more specifically, atherosclerosis refers to the buildup of cholesterol and fats in the artery walls.

[9] Several genetic pathways that lead to apoptosis of kidney cells have been implicated in mice models and in-vitro assays.

[12] Activation of pro-caspase 8 initiates apoptosis via signaling from cell-surface death receptors such as Fas proteins and their ligands FADD and DAXX.

Upregulation of Fas and FADD protein has occurred in mice models after a 24h period of ischemic injury.

This shows that the Fas-pathway may play a role in the pathogenesis of the apoptosis of tubule cells during the early ischemic-reperfusion period.

Activation of Bcl-2 proteins such as Bax and Bak triggers a signaling cascade that results in the release of cytochrome c into the cytosol.

Similarly to the APO-E polymorphism, patients with the D-allele for ACE has an increased risk of acute kidney injury after coronary artery bypass grafting, as well.

[12] In infant studies, it was shown that HSP72 gene with the G allele gave an increased risk for acute kidney injury.

Moreover, Knockout variants of the IL-17C decreased the inflammation caused by activation of IL-17C.Using antibodies and siRNA against IL-17C also provided the same results.

[12] Unlike with HSP72 polymorphism, infant studies show that VEGF with a homozygous A allele resulted in reduced risk for acute kidney injury.

This includes changes in the vasculature, endoplasmic reticulum stress, disfunction of the mitochondria, autophagy of cells, inflammation, and incorrect or maladaptive repair.

When that happens, the kidney undergoes oxidative stress and injury to the microvascular endothelium promotes the recruitment of leukocytes and platelets.

This leads to the mitochondria releasing pro-apoptotic proteins such as cytochrome c and end up in the death of kidney cells.

The process of autophagy helps in removing unnecessary components of the cells to maintain more important functions.

[15] When the kidneys undergo inflammatory responses, it produces mediators such as bradykinin, histamine, and pro-inflammatory cytokines such as interleukin-1 and tumor necrosis factor-a.

[15] When an injury is severe, the adaptive responses that are activated to restore normal cell and tissue homeostasis become maladaptive.

[16] Likewise above, patients who are being treated with an antihypertensive drug for renovascular, refractory or severe hypertension exhibit progressive azotemia.

[16] Acute kidney ischemia may result from taking ACEIs due to the alteration of intrarenal hemodynamics.

Duplex Doppler Sonography(DDS) is an imaging test for evaluating blood flow in the kidney or the renal system.

More clinical uses of MRA is used to check blood vessels in different parts of the body, such as the thorax, lower limbs, and the heart.

This assay measures the activity of renin, also known as angiotensinogenase, which plays a role in blood pressure regulation and urine output.

By performing this scan, doctors can differentiate between kidney ischemia and intrinsic renal disease by checking the amount of time for the radioactivity to peak and decline.

Based on these studies, kidney transplants and retrospective partial nephrectomy series indicate the risk of renal function impairment the longer the ischemic injury persists.

[29] However, based on historical studies, the use of the duration of the ischemia as a dichotomous marker has been found to have significant flaws in predicting renal function outcomes.

Taking furosemide as a tablet, as a liquid solution, or via injection is used as a preventative measure or as treatment of kidney ischemia has shown to reduce the severity of renal failure, reduce apoptosis induced by ischemia, and speed the recovery of renal function.

Chronic ischemic kidney disease (CIKD) usually involves loss of renal parenchyma or reduction of GFR caused by gradual vascular obstruction.