Chronic kidney disease: Case Study

Chronic kidney disease: Case Study

Introduction

Chronic kidney disease (CKD) is a venerable, increasing decline of the functions of kidneys. The warning signs and symptoms build up gradually and comprise of vomiting, nausea, dysguesia, anorexia, fatigue, nocturia, pruritis, stomatitis, lassitude, reduced psychological perception, cramps and twitches in muscles, retention of water, under nutrition, gastro intestinal bleeding and ulceration, neuropathies in peripheries, and fits. Detection is derived from the investigative trials of function of kidney in laboratory, occasionally accompanied by the biopsy of kidneys. Management and cure is initially based on the casual status but takes in the management of electrolytes and fluids, anemic erythropoietin, and dialysis or renal transplant often.

Chronic kidney disease, which is also known as chronic renal disease, may come out because of any reason of dysfunction of kidney with adequate extent. In United States, one of the general reasons of renal disease is “Diabetic Neuropathy”, subsequent to “Hypertensive Nephro-angio-sclerosis” and a range of initial and subsequent “Glomerulo-pathies”. An outsized and increasing reason of the damage of kidneys is “Metabolic Syndrome”' wherein diabetes type II and hypertension are in attendance (Zandi-Nejad, Luyckx & Brenner, 2006).

Discussion

Pathophysiology of Chronic Kidney Disease

When renal blood flow decreases, the basic driving force filtration also reduces (Wang & Hirschberg, 2000). Also, the kidneys no longer receive oxygen and other nutrients vital to the cellular metabolism. As a result of the decrease in glomerular filtration is waste products accumulate in the body and therefore, the patient will experience increase in serum creatinine and BUN (blood urea nitrogen), which is called azotemia. To avoid renal hypoperfusion requiring kidney Mean arterial pressure of at least 60-70 mmHg, in case of not reaching this pressure the kidneys are launched two important adaptive responses: Autoregulation: Keeps glomerular hydrostatic pressure through the expansion of the afferent arteriole and constriction of the efferent arteriole saw increases blood flow in the glomerular capillary bed and delaying the output of blood from same, obtaining a pressure increase and the velocity of glomerular filtration (Jan Brod, 2009).

Activation of the renin-angiotensin-aldosterone system: This system stimulates peripheral vasoconstriction, which in turn increases the perfusion pressure by stimulating aldosterone secretion resulting in the re-absorption of sodium and water and secretion of potassium. Re-absorption of sodium and water increases the total intravascular volume improving perfusion of the kidneys. Sodium re-absorption leads to an increase plasma osmolality, which in turn stimulates the release of antidiuretic hormone (ADH), which promotes water re-absorption at the distal tubules (Jan Brod, 2009). The evolution of the IRA is divided into four phases:

Beginning of assault or injury: This phase is important because if you act immediately possible to solve or prevent subsequent renal dysfunction. This phase can last from hours to days. At this stage uremic symptoms appear.

Phase oliguric: Oliguria is the first symptom to appear in this disease, puediendo last from 8 to 14 days. At this stage the urine output is diminished dramatically (below 400 ml / day)

Diuretic phase: usually lasts about 10 days and said ...