Renin

Name: Adult Polycystic Kidney Disease AKA: Autosomal Dominant Polycystic Kidney Disease (ADPKD) – Common Organ: Cysts form in the proximal convoluted tubules, Bowman’s capsule and collecting ducts of the kidneys. With time, the cysts enlarge. Patients can also present with cysts in the liver, pancreas, lungs, spleen, ovaries, seminal vesicles, testes, epididymis, thyroid, uterus, and bladder. Labs: Proteinuria (50% of patients), azotemia, hematuria, anemia Signs and Symptoms: Abdominal and lumbar pain, HTN Sonographically: Bilateral, enlarged kidneys. Renal capsule is poorly outlined and distorted central echogenic renal sinus due to numerous variable sized cysts throughout cortex. Complications: Infection, renal calculi, cyst rupture, hemorrhage, ureteric obstruction, and tends to cause kidney failure. Patients can remain asymptomatic until their 40s. Death usually occurs about 10 years after onset of symptoms. The most common causes of death are uremia (59%), cerebral hemorrhage (13%) and cardiac disease associated with HTN. Page Numbers: 289 and 291 Name: Medullary Sponge Kidney AKA: Tubular Ectasia – Autosomal recessive - common Organ: Bilateral kidneys – multiple cystic dilatation of the collecting ducts in the medulla. Labs: Usually normal Signs and Symptoms: Usually asymptomatic, however pain, hydronephrosis, infection and urinary calculi may develop. Sonographically: Bilateral hyperechoic medullary pyramids without acoustic shadowing with possible calculi.…

There are multiple kidney diseases that are known to the Medical world, but there will be a discussion about Henoch Shönlein Purpura today. Many young kids have had this Kidney disease and it is not to be taken lightly. At first it comes off as something simple, and it looks like the victim has probably just pulled a muscle, has a fever or has a stomach ache because they are vomiting but no, that is just the beginning of this horrid kidney disease. There are probably many questions going around…

505). Sodium is reabsorbed in the proximal tubule and loop of Henle regardless of sodium load. Aldosterone is the main factor when kidneys determine the rate of sodium reabsorption. Aldosterone causes an increase in sodium reabsorption. Aldosterone is usually secreted by the adrenal cortex when plasma volume is low. It is controlled by angiotensin II, a component of the renin-angiotensin system. Renin, an enzyme that is secreted by the granular cells in the Juxtaglomerular apparatus (JGA),…

One of the causes on systematic level is renal artery stenosis. This is the narrowing of the arteries that transport blood to the kidney. Since the arteries are narrowed they bring in less blood to the kidney. This causes the kidney to sense a lower blood volume. When this happens the kidney will release the enzyme, Renin. This enzyme will convert angiotensinogen, which is secreted by the liver, to angiotensin I. When the lungs sense angiotensin I in the circulation they will release…

Renin secretion is stimulated by decreased blood volume, decreased renal perfusion, sodium and water depletion. Subsequently, renin promotes the conversion of angiotensinogen to angiotensin I. Angiotensin I is then converted to angiotensin II through the angiotensin converting enzyme. Due to angiotensin II being a potent vasoconstrictor, it also stimulates aldosterone secretion leading to sodium and water retention. The subsequent renal retention of sodium and water, coupled with an increase in…

According to the American Pharmacists Association, as of late July, Alirocumab, a PCSK9 inhibitor, obtained FDA approval. In addition to diet and aggressive statin therapy, Alirocumab acts as an aid for patients that have clinical atherosclerotic cardiovascular disease or heterozygous familial hypercholesterolemia. These patients are required to lower their cholesterol further. Alirocumab, a monoclonal antibody which is self-administered through subcutaneious injection every two weeks, lowers…

vascular walls or macula dense cells detect a change and renin is released into the bloodstream. Renin by itself cannot affect blood pressure until it binds with inactive angiotensin and forms angiotensin II through the use of the angiotensin-converting enzyme. The final product of angiotensin II causes blood pressure levels to increase due to blood vessel constriction, as well as the release of aldosterone into the arterial glands which results in sodium and water retention and potassium…

Extra if needed Diagnosis of PAI initially involves blood assay for elevated ACTH and plasma renin activity (PRA) with decreased serum cortisol and aldosterone, DHEAS [1, 2]. Exclusion of other autoimmune conditions and imaging of the adrenal glands completes diagnostic testing and results [3]. Diagnostic Testing and Results Optimal levels of serum cortisol and plasma ACTH are simultaneously measured early morning between 8-9am, in healthy individuals the serum cortisol levels can range…

cardiac output but their peripheral resistance is elevated. Peripheral resistance occurs when the smooth muscle cells of the small arterioles contract which occurs due to an increase in intracellular calcium concentrations. If this problem is not is not addressed then it can lead to thickening of the arteriolar vessel walls causing an irreversible rise in the peripheral vascular resistance. The renin-angiotensin system is an important part of the endocrine system in maintaining blood pressure.…

development and of hypertension is the renal sympathetic nervous system, and it affects the blood pressure via 2 pathways the efferent and afferent pathways: The efferent pathway carries signals from the SNS to the kidney and increases renin release thereby activating the RAAS system and increasing sodium and water retention, all resulting in increased circulating volumes and therefore increased blood pressures. In addition to the previously mentioned processes the efferent pathway also…