Several pathophysiological conditions that change when the<unk>  is undergoing<unk>  injuries are listed below. This includes changes in the vasculature, endoplasmic reticulum stress, disfunction of the mitochondria, autophagy of cells, inflammation, and incorrect or maladaptive repair. Vasculature Normal functions of the<unk>  require a high amount of oxygen, as such the Oxygen supply to the<unk>  is well regulated. Production of Adenosine Triphosphate and Nitric Oxide requires a high concentration of Oxygen. These compounds, as well as some reactive oxygen species, are required for the<unk>  to function properly. With an injury, cellular respiration is compromised. This leads to an imbalance of the supply of oxygen and the products of cellular respiration. When that happens, the<unk>  undergoes oxidative stress and injury to the microvascular endothelium promotes the recruitment of leukocytes and platelets. This leads to changes in perfusion and oxygen delivery. Endoplasmic Reticulum Stress Misfolded and unfolded proteins accumulate in the endoplasmic reticulum. This triggers the unfolded protein response (UPR). The unfolded protein response is an adaptive mechanism to restore cell and tissue homeostasis. If the stress is too severe, the maladaptive response is activated and the C/EBP Homologous Protein pathway (CHOP) is induced. This leads to apoptosis. Mitochondrial Dysfunction In acute<unk> , the proximal tubules are vulnerable to mitochondrial dysfunction because they rely on aerobic metabolism and they are in a more oxidized state as compared to the distal tubules. When mitochondrial dysfunction happens, cellular respiration is disrupted. This leads to the mitochondria releasing pro-apoptotic proteins such as cytochrome c and end up in the death of<unk>  cells. Autophagy During<unk>  stress, the cross-talk between the mitochondria and the UPR is activated. This results in autophagy by which proteins, organelles, and cytoplasmic components are recycled and degraded by the lysosomes. The process of autophagy helps in removing unnecessary components of the cells to maintain more important functions. In this case, autophagy is induced in<unk> s in response to hypoxia to protect against further<unk>  injury. Inflammation The renal inflammatory process involves events that lead to injury or death of renal cells. When the<unk> s undergo inflammatory responses, it produces mediators such as bradykinin, histamine, and pro-inflammatory cytokines such as interleukin-1 and tumor necrosis factor-a. In mice models, studies wherein removal of these mediators from plasma were observed and has shown beneficial to mice. Maladaptive Repair When an injury is severe, the adaptive responses that are activated to restore normal cell and tissue homeostasis become maladaptive. This leads to cell and tissue malfunction. This could lead to chronic<unk>  disease progression. Physical Symptoms Physical symptoms implicated with<unk>  includes<unk>  shrinkage or a difference in<unk>  sizes, renovascular hypertension, acute renal failure, progressive azotemia, diagnosed by an increase of nitrogen compounds in urine, and acute pulmonary edema which is excess fluid in the lungs. This diagram is drawn using BioRender.com<unk>  features can be clinically suggestive of renal<unk> . Because renal failure can be correlated to hypertension, both of these situations have been observed. In general,<unk>  sizes differ in patients with acute<unk> . Hypertension, acute renal failure, progressive azotemia, and acute pulmonary edema are also signs of a developing<unk>  injury for hypertensive patients.<unk>  size differences In normal patients, the length of the two<unk> s only differ by less than 1.5 cm; however, hypertensive patients tend to have an asymmetric<unk>  size. This strongly suggests<unk>  renal disease. Renovascular hypertension Renovascular hypertension or renal artery stenosis is characterized as an increase in blood pressure through the arteries to the<unk> s. This is due to an abnormal narrowing of the arteries. Acute Renal Failure caused by the treatment of hypertension In patients with hypertension, treatment of the disease using Angiotensin-converting enzyme inhibitors (ACEIs) are sometimes necessary. The glomerular filtration rate(GFR) in patients is regulated by vasoconstriction of the efferent arteriole. When ACEI is taken by the patient, this vasoconstrictor effect of the efferent arteriole is blocked. This then leads to a decrease in GFR and leads to acute renal failure. Studies have shown that 6-38% of patients with renal vascular disease or hypertension will develop acute renal<unk>  through acute renal failure. Progressive Azotemia (with Renovascular Hypertension, refractory or severe hypertension, or atherosclerotic diseases) Azotemia is characterized as an increase of creatinine and blood urea nitrogen (BUN) in the plasma. Patients who have renovascular hypertension often get a deterioration of the renal function. Likewise above, patients who are being treated with an antihypertensive drug for renovascular, refractory or severe hypertension exhibit progressive azotemia. Acute<unk>  may result from taking ACEIs due to the alteration of intrarenal hemodynamics. Acute pulmonary edema Acute pulmonary edema is characterized as a fluid collection in the air sacs of the lungs. This makes it difficult for patients to breathe. Patients with poorly-controlled hypertension and renal insufficiency usually also have recurrent acute pulmonary edema. While patients may have other risk factors for having pulmonary edema, volume-dependent renovascular hypertension appears to be the dominant factor.
Kidney ischemia
Renal ischemia
Renal colic
Pyonephrosis
Renal papillary necrosis
Obstructive uropathy
Renal cortical necrosis
Acute kidney injury