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For a US perspective, see the KDOQI clinical practice guidelines [10] and for a United Kingdom perspective see: U.K. Renal Association clinical practice guidelines [11] According to the US guidelines, for thrice a week dialysis a Kt/V (without rebound) should be 1.2 at a minimum with a target value of 1.4 (15% above the minimum values). However ...
S and V differ markedly between small vs. large people and between men and women. A man and a woman of the same S will have similar levels of GFR, but their values for V may differ by 15-20%. Because standardized Kt/V incorporates residual renal function into the calculations, it makes the assumption that kidney function should scale by V.
The specific gene is not identified. While biochemically similar, type 1 and 2 disease may be distinguished by the differing urinary excretion of cyclic AMP in response to exogenous PTH. [citation needed] Some sources also refer to a "type 1c" (OMIM 612462). [9] The phenotype is the same as in type 1a, but red blood cells show normal Gs activity.
The normal range of GFR, adjusted for body surface area, is 100–130 average 125 (mL/min)/(1.73 m 2) in men and 90–120 (mL/min)/(1.73 m 2) in women younger than the age of 40. In children, GFR measured by inulin clearance is 110 (mL/min)/(1.73 m 2 ) until 2 years of age in both sexes, and then it progressively decreases.
PTH normally inhibits reabsorption of phosphate by the kidney. Therefore, without enough PTH there is more reabsorption of the phosphate leading to a high phosphate level in the blood. [citation needed] Chronic kidney failure: When the kidneys are not working well, there will be increased phosphate retention. [citation needed]
If this is successful, PTH levels return to normal levels, unless PTH secretion has become autonomous (tertiary hyperparathyroidism). [50] Hyperphosphatemia may be treated by decreasing dietary intake of phosphate. If phosphate remains persistently elevated above 5.5 mg/dL with dietary restriction, then phosphate binders may be used. [55]
Pseudopseudohypoparathyroidism (PPHP) is an inherited disorder, [1] named for its similarity to pseudohypoparathyroidism in presentation. It is more properly Albright hereditary osteodystrophy, although without resistance of parathyroid hormone (PTH), as frequently seen in that affliction.
The main symptoms of hypoparathyroidism are the result of the low blood calcium level, which interferes with normal muscle contraction and nerve conduction.As a result, people with hypoparathyroidism can experience paresthesia, an unpleasant tingling sensation around the mouth and in the hands and feet, as well as muscle cramps and severe spasms known as "tetany" that affect the hands and feet ...