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See Treatment and Medication for more detail. For a discussion of CKD in children, click here. Pathophysiology 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 etiologythe 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. For example, a rise in plasma creatinine from a baseline value of 0. 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 [NSAIDs], intravenous contrast media Decreased perfusion eg, from severe dehydration or episodes of shock Proteinuria in addition to being a marker of CKD Hyperlipidemia Hyperphosphatemia with calcium phosphate deposition Smoking Uncontrolled diabetes Thaker et al found a strong association between episodes of acute kidney injury AKI and cumulative risk for the development of advanced CKD in multiple hospitalized patients with diabetes mellitus.
Childhood renal function and CKD in children In children, the GFR increases with age and is calculated with specific equations that are different than those for adults.
Adjusted for body surface area, the GFR reaches adult levels by age 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. Advances in pediatric nephrology have enabled great leaps in survival for pediatric CKD and end-stage renal disease ESRDincluding 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. 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. 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. 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 levels are an independent risk factor for ESRD in patients who have fairly well-preserved kidney function stages and for mortality across the scope of CKD.
This study also suggests a separate genetic influence on development of albuminuria versus reduction in GFR.
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 can be observed sooner in patients who ingest a potassium-rich diet or have low serum aldosterone levels.
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.Chronic disease was defined as any disease under the Ministry of Health’s Chronic Disease Management Program (CDMP).
19 Patients with documented history of cognitive impairment or dementia, or who were incapable of understanding and communicating in English were excluded. Older adults were defined as individuals age 65 years and above at the.
Chronic lower respiratory diseases, such as chronic obstructive pulmonary disease, are the third most common cause of death among people 65 and older, with , deaths in , according to.
Nov 19, · GoalImprove the health, function, and quality of life of older alphabetnyc.comewAs Americans live longer, growth in the number of older adults is unprecedented.
In , % ( million) of the US population was aged 65 or older and is projected to reach % (98 million) by Aging adults experience higher risk of chronic disease. Chronic disease: A disease that persists for a long time. A chronic disease is one lasting 3 months or more, by the definition of the U.S.
National Center for Health Statistics. A chronic disease is one lasting 3 months or more, by the definition of the U.S. National Center for Health Statistics. PREVALENCE OF CHRONIC DISEASES AMONG THE AGED IN CAPE COAST METROPOLITAN OVER LAST FOUR YEARS Introduction This paper charts a brief history of Ghana’s chronic disease burden over the last five years, focusing on prevalence, risk and illness implications in relation to aging.
Chronic Conditions Among older Americans Chronic illness on the rise How much Do We Spend on Chronic Conditions? A Closer look at Selected Chronic Conditions. 10 chronic cAre: A CAll to ACtion for HEAltH rEform a chronic disease.
“more than 70 million Americans ages 50 and.