Chronic Kidney Disease: Practice Essentials, Pathophysiology, Etiology. A normal kidney contains approximately 1 million nephrons, each of which contributes to the total glomerular filtration rate (GFR). In the face of renal injury (regardless of the etiology), the kidney has an innate ability to maintain GFR, despite progressive destruction of nephrons, as the remaining healthy nephrons manifest hyperfiltration and compensatory hypertrophy. This nephron adaptability allows for continued normal clearance of plasma solutes. Plasma levels of substances such as urea and creatinine start to show measurable increases only after total GFR has decreased to 5. The plasma creatinine value will approximately double with a 5. GFR. For example, a rise in plasma creatinine from a baseline value of 0. L to 1. 2 mg/d. L in a patient, although still within the adult reference range, actually represents a loss of 5. The hyperfiltration and hypertrophy of residual nephrons, although beneficial for the reasons noted, has been hypothesized to represent a major cause of progressive renal dysfunction. The increased glomerular capillary pressure may damage the capillaries, leading initially to secondary focal and segmental glomerulosclerosis (FSGS) and eventually to global glomerulosclerosis. This hypothesis is supported by studies of five- sixths nephrectomized rats, which develop lesions identical to those observed in humans with chronic kidney disease (CKD). Factors other than the underlying disease process and glomerular hypertension that may cause progressive renal injury include the following: Systemic hypertension. Nephrotoxins (eg, nonsteroidal anti- inflammatory drugs . Adjusted for body surface area, the GFR reaches adult levels by age 2- 3 years. Aspects of pediatric kidney function and the measure of creatinine are informative not only for children but also for adults. For example, it is important to realize that creatinine is derived from muscle and, therefore, that children and smaller individuals have lower creatinine levels independent of the GFR. Consequently, laboratory reports that do not supply appropriate pediatric normal ranges are misleading. The same is true for individuals who have low muscle mass for other reasons, such as malnutrition, cachexia, or amputation. Another important note for childhood CKD is that physicians caring for children must be aware of normal blood pressure levels by age, sex, and height. Prompt recognition of hypertension at any age is important, because it may be caused by primary renal disease. Fortunately, CKD during childhood is rare and is usually the result of congenital defects, such as posterior urethral valves or dysplastic kidney malformations. Another common cause is FSGS. Genetic kidney diseases are also frequently manifested in childhood CKD. The Vegetarian Diet and CKD Stage 3 2016-01-12 01:50. For stage 3 CKD, it is very necessary and important to have a restricted diet in life, which is good for.Stage 3 CKD can affect your bones, so your physician may recommend limiting your phosphorus intake because excess phosphorus can rob the bones. Stage 4 CKD is severely reduced kidney function, 15-30% (eGFR 15-29ml/min/1.73m 2) Stage 5 CKD is very severely reduced kidney function (endstage or ESRF/ESRD), less. 5 Diet Guidelines for Stage 5 CKD Non-Dialysis Patients. Disclaimer: This article is for informational purposes only and is not intended to be a substitute for. Stage 3 Kidney Failure is characterized by moderate kidney damage. There are five stages of Chronic Kidney Disease, according to the glomerular filtration rate (GFR). Chronic kidney disease is defined as kidney disease that has been present for months to years. Chronic renal disease (CRD), chronic renal failure (CRF), and chronic. Chronic kidney disease (CKD) associated with type 2 diabetes is the leading cause of kidney failure, with both inflammation and oxidative stress. Advances in pediatric nephrology have enabled great leaps in survival for pediatric CKD and end- stage renal disease (ESRD), including for children who need dialysis or transplantation. Aging and renal function. The biologic process of aging initiates various structural and functional changes within the kidney. Histologic examination is notable for a decrease in glomerular number of as much as 3. The GFR peaks during the third decade of life at approximately 1. L/min/1. 7. 3 m. 2; it then undergoes an annual mean decline of approximately 1 m. L/min/y/1. 7. 3 m. L/min/1. 7. 3 m. 2 at age 7. Ischemic obsolescence of cortical glomeruli is predominant, with relative sparing of the renal medulla. Juxtamedullary glomeruli see a shunting of blood from afferent to efferent arterioles, resulting in redistribution of blood flow favoring the renal medulla. These anatomic and functional changes in renal vasculature appear to contribute to an age- related decrease in renal blood flow. Renal hemodynamic measurements in aged humans and animals suggest that altered functional response of the renal vasculature may be an underlying factor in diminished renal blood flow and increased filtration noted with progressive renal aging. The vasodilatory response is blunted in the elderly when compared to younger patients. However, the vasoconstrictor response to intrarenal angiotensin is identical in young and older human subjects. A blunted vasodilatory capacity with appropriate vasoconstrictor response may indicate that the aged kidney is in a state of vasodilatation to compensate for the underlying sclerotic damage. Given the histologic evidence for nephronal senescence with age, a decline in the GFR is expected. However, a wide variation in the rate of GFR decline is reported because of measurement methods, race, gender, genetic variance, and other risk factors for renal dysfunction. Genetics. Most cases of CKD are acquired rather than inherited, although CKD in a child is more likely to have a genetic or inherited cause. Well- described genetic syndromes associated with CKD include autosomal dominant polycystic kidney disease (ADPKD) and Alport syndrome. Other examples of specific single- gene or few- gene mutations associated with CKD include Dent disease, nephronophthisis, and atypical hemolytic uremic syndrome (HUS). APOL1 gene. More recently, researchers have begun to identify genetic contributions to increased risk for development or progression of CKD. Chronic Kidney Disease can be divided into five stages according to the level of GFR. It means the kidney function decreases gradually with time going. Stage 2 of Chronic Kidney Disease. A person with stage 2 chronic kidney disease (CKD) has kidney damage with a mild decrease in their glomerular filtration rate (GFR. Friedman et al found that more than 3 million black persons with genetic variants in both copies of apolipoprotein L1 (APOL1) are at higher risk for hypertension- attributable ESRD and FSGS. In contrast, black individuals without the risk genotype and European Americans appear to have similar risk for developing nondiabetic CKD. Isakova et al reported that elevated FGF- 2. ESRD in patients who have fairly well- preserved kidney function (stages 2- 4) and for mortality across the scope of CKD. This study also suggests a separate genetic influence on development of albuminuria versus reduction in GFR. Many of these genes involve aspects of the immune system (eg, CCR3, IL1. RN, IL4). One study found that patients with CKD were significantly more likely to have the A2. G polymorphism in the ACE gene, which encodes the angiotensin- converting enzyme (ACE). Another defense against potassium retention in patients with CKD is increased potassium excretion in the gastrointestinal tract, which also is under control of aldosterone. Hyperkalemia usually does not develop until the GFR falls to less than 2. L/min/1. 7. 3 m. Hyperkalemia can be observed sooner in patients who ingest a potassium- rich diet or have low serum aldosterone levels. Common sources of low aldosterone levels are diabetes mellitus and the use of ACE inhibitors, NSAIDs, or beta- blockers. Hyperkalemia in CKD can be aggravated by an extracellular shift of potassium, such as occurs in the setting of acidemia or from lack of insulin. Hypokalemia. Hypokalemia is uncommon but can develop in patients with very poor intake of potassium, gastrointestinal or urinary loss of potassium, or diarrhea or in patients who use diuretics. Metabolic acidosis. Metabolic acidosis often is a mixture of normal anion gap and increased anion gap; the latter is observed generally with stage 5 CKD but with the anion gap generally not higher than 2. Eq/L. In CKD, the kidneys are unable to produce enough ammonia in the proximal tubules to excrete the endogenous acid into the urine in the form of ammonium. In stage 5 CKD, accumulation of phosphates, sulfates, and other organic anions are the cause of the increase in anion gap. Metabolic acidosis has been shown to have deleterious effects on protein balance, leading to the following: Negative nitrogen balance. Increased protein degradation. Increased essential amino acid oxidation. Reduced albumin synthesis. Lack of adaptation to a low- protein diet. Hence, metabolic acidosis is associated with protein- energy malnutrition, loss of lean body mass, and muscle weakness. Know the dangers of chronic kidney disease in cats, its symptoms and how you can save your beloved feline from acquiring it. The mechanism for reducing protein may include effects on adenosine triphosphate (ATP)–dependent ubiquitin proteasomes and increased activity of branched- chain keto acid dehydrogenases. Metabolic acidosis also leads to an increase in fibrosis and rapid progression of kidney disease, by causing an increase in ammoniagenesis to enhance hydrogen excretion. In addition, metabolic acidosis is a factor in the development of renal osteodystrophy, because bone acts as a buffer for excess acid, with resultant loss of mineral. Acidosis may interfere with vitamin D metabolism, and patients who are persistently more acidotic are more likely to have osteomalacia or low- turnover bone disease. Salt- and water- handling abnormalities. Salt and water handling by the kidney is altered in CKD. Extracellular volume expansion and total- body volume overload results from failure of sodium and free- water excretion. This generally becomes clinically manifested when the GFR falls to less than 1. L/min/1. 7. 3 m. At a higher GFR, excess sodium and water intake could result in a similar picture if the ingested amounts of sodium and water exceed the available potential for compensatory excretion. Tubulointerstitial renal diseases represent the minority of cases of CKD. However, it is important to note that such diseases often cause fluid loss rather than overload. Thus, despite moderate or severe reductions in GFR, tubulointerstitial renal diseases may manifest first as polyuria and volume depletion, with inability to concentrate the urine. These symptoms may be subtle and require close attention to be recognized. Volume overload occurs only when GFR reduction becomes very severe. Anemia. Normochromic normocytic anemia principally develops from decreased renal synthesis of erythropoietin, the hormone responsible for bone marrow stimulation for red blood cell (RBC) production. The anemia starts early in the course of the disease and becomes more severe as, with the shrinking availability of viable renal mass, the GFR progressively decreases. An error occurred while setting your user cookie. Please set your. browser to accept cookies to continue. This cookie stores just a. ID; no other information is captured. Accepting the NEJM cookie is.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. Archives
July 2017
Categories |