Kidney disease, chronic glomerular filtration rate

Chronic Kidney Disease Detection. Chronic kidney disease is detected by a blood analysis for levels of creatinine. Higher levels of creatinine indicate a decreased glomerular filtration rate resulting in a decline in normal kidney function. A glomerular filtration rate of less than 60 milliliters per minute per 1.73 nP, for a period of three months, is classified as having chronic kidney disease. Red blood cells or excess protein detected in urinalysis may cause a physician to investigate more thoroughly. 

Chronic kidney disease (CKD) is increasingly recognized as a major public health problem. Defined as an irreversible progressive loss of renal function for 3 months or longer, CKD shows a glomerular filtration rate (GFR) less... 

Different methods of kidney imaging have shown that Balkan nephropathy patients with chronic renal failure have symmetrically shrunken kidneys with smooth surface and no calcifications [90]. The time at which the shrinking occurs remains to be determined. While some authors suggest that the size of the kidneys remains normal in patients in the latent phase of the disease and with normal renal function, others report cases of shrunken kidneys in patients in an early phase with normal glomerular filtration rate, and it was even proposed that the disease was characterized with primarily small kidneys [98, 110, 112]. As ultrasound became a standard imaging method in the evaluation of kidney dimensions, several recent studies that used this method showed diminished kidney length and cortex width in members of Balkan nephropathy families with normal kidney function [113, 114]. Besides,... 

Chronic renal failure is treated by dialysis, kidney transplants, and drugs, as well as by low-protein diets. For this reason, an outline of chronic renal failure occurs in this chapter. The normal glomerular filtration rate (GFR) is 80 to 120 ml/min. In severe renal disease, the GFR can be reduced to 10 ml/min or less. This represents a 90% loss of renal function. Diabetes mellitus and hypertension (high blood pressure) are the main causes of chronic renal failure. Sustained and chronic injury to the kidneys leads to the destruction of the nephrons, where this destruction is usually not reversible. The nephron, which is the smallest unit of kidney function, is detailed in the section on Sodium, Potassium, Chloride, and Water. The severe loss of nephrons results in alterations of functions of many other organs of the body. The collection of abnormalities that results is called uremia. 

Patients with hypertension may develop damage to either the renal tissue (parenchyma) or the renal arteries. Chronic kidney disease presents initially as microalbuminuria (30-299 mg albumin in a 24-hour urine collection) that can progress to macroalbuminuria and overt kidney failure. The rate of kidney function deterioration is accelerated when both hypertension and diabetes are present. Once patients have an estimated glomerular filtration rate (GFR) of less than 60 mL/m per minute or macroalbuminuria, they have chronic kidney disease, and the risk of cardiovascular disease and progression to severe chronic kidney disease increases. Strict BP control to a goal of less than 130/80 mm Hg can slow the decline in kidney function. This strict control often requires two or more antihypertensive agents. 

CHAPTER 43 CHRONIC KIDNEY DISEASE PROGRESSION-MODIEYING THERAPIES 809 TABLE 43—4. Effects of Anti hypertensive Agents on Renal Blood Flow (RBF) and Glomerular Filtration Rate (GFR)... 

Ca X P calcium phosphorus product serum calcium multiplied by serum phosphorus CKD chronic kidney disease CPK creatine phosphokinase DEO deferoxamine EPO erythropoietin ESKD end-stage kidney disease ESRD end-stage renal disease FEk fractional excretion of potassium FEn fractional excretion of sodium GFR glomerular filtration rate Hct hematocrit HDL high-density fipoprotein Hgb hemoglobin... 

The most common cause of hyperphosphatemia is a decrease in urinary phosphorus excretion secondary to decreased glomerular filtration rate. ° Retention of phosphorus decreases vitamin D synthesis and induces hypocalcemia, which leads to an increase in PTH. This physiologic response inhibits further tubular reabsorption of phosphorus to correct hyperphosphatemia and normalize serum calcium concentrations. Patients with excessive exogenous phosphorus administration or endogenous intracellular phosphorus release in the setting of acute renal failure may develop profound hyperphosphatemia. Severe hyperphosphatemia is commonly encountered in patients with chronic kidney disease, especially those with GFRs less than 15 mL/ min per 1.73 m (see Chap. 44). 

Chronic kidney disease (CKD), as evidenced by the inability of the kidneys to excrete nitrogenous and other waste products, usually develops over months to years (see Chap. 43). Malnutrition secondary to reduced oral nutrient intake frequently is evident when the glomerular filtration rate (GFR) drops below 20 to 25 mL/min. Patients with CKD are considered to have ESKD when the GER falls below 15 mL/min (see Chap. 44). Malnutrition is also a common occurrence in ESKD, not only because of decreased oral intake, but also due to increased nutrient losses via the various renal replacement therapies. Because of its chronicity, malnutrition in these patients is treated most frequently in the ambulatory setting with EN. 

Chronic renal failure (CRF) is the progressive irreversible destruction of kidney tissue by disease which, if not treated by dialysis or transplant, will result in the death of the patient. The aetiology of CRF encompasses the spectrum of known kidney diseases. The end result of progressive renal damage is the same no matter what the cause of the disease may have been. The major effects of renal failure all occur because of the loss of functioning nephrons. It is a feature of CRF that patients may have few if any symptoms until the glomerular filtration rate falls below 15 ml/min (i.e. to 10% of normal function), and the disease is far advanced. 

Renal effects of hypercalcemia include reduced glomerular filtration rate (GFR), polyuria, nephrocalcinosis, and renal stone disease. Hypercalcemia causes renal vasoconstriction which may contribute to decreased GFR. The hypercalcemia-induced polyuria results from 1) an impairment of active transport of NaCl in the loop of Henle, distal tubule and collecting duct and 2) an inhibition of vasopressin-facilitated absorption of water in the distal nephron. As a direct result of the polyuria, many side effects including polydipsia, thirst, nocturia and dehydration are common. Precipitation of calcium salts within the kidney leads to chronic inflammatory reactions (nephrocalcinosis), fibrosis, renal impairment, nephrolithiasis and urolithiasis. Further renal damage may occur indirectly from hypertension. 

Electrolyte balance Concern about the risk of hyperkalemia associated with ACE inhibitors in patients with chronic kidney disease probably inhibits their use in such patients despite the beneficial effects of ACE inhibitors on progression of chronic kidney disease. In 1094 non-diabetic African-American adults with hypertensive chronic kidney disease, hyperkalemia was associated with increasing age, baseline protein excretion, glomerular filtration rate (GFR), and baseline potassium concentrations. Use of a potassium-wasting diuretic reduced the risk of hyperkalemia [36 ]. 

Chronic kidney disease is a known cardiovascular risk factor. However, certain therapies may not be suitable for investigation in individuals with kidney disease because a reduced glomerular filtration rate may result in accumulation of the drug and/or its metabolites. This limitation may exclude individuals with moderate to severe kidney disease from participating in certain trials, or may necessitate a trial to be conducted solely in these individuals to assess the drug s safety and efficacy in this population. 

Chronic renal failure is known to be associated with an accelerated process of atherosclerosis. Importantly, cardiovascular disease is the main cause of morbidity and mortality with CKD and kidney transplant recipients. High serum phosphate levels have been shown to be associated with higher mortality for all causes, cardiovascular mortality and vascular calcification (Block et al. 2004 Young et al. 2004). Phosphorus retention develops in CKD when the glomerular filtration rate (GFR) falls below 25 ml/min. It was estimated that for each 1 mg/dl of serum phosphate increase in CKD, the risk of having myocardial infarction increases by 35% (Kestenbaum et al. 2005). 

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