Renal filtration threshold

PEG (20 kDa) [43]. This demonstrates the strong hydrodynamic properties of PEGylated molecules. The increase in hydrodynamic radius significantly decreases renal clearance. Although the threshold of the molecular weight cut-off of renal filtration of protein is about 65 kDa, the 30-kDa PEG demonstrates minimal renal permeability [44]. 

Hyperphosphatemia is usually secondary to the inability of the kidneys to excrete phosphate. In acute or chronic renal failure, a decrease in glomerular filtration rate (GFR) reduces the renal excretion of phosphate, resulting in hyperphosphatemia. Moderate increases of serum phosphate occur in individuals with low PTH (hypoparathyroidism), PTH resistance (pseudohypoparathyroidism), or acromegaly (increased growth hormone) caused by an increased renal phosphate threshold. Growdi hormone is responsible for the increased renal phosphate threshold and higher phosphate concentrations observed in children. EDTA therapy has also been associated with hyperphosphatemia. 

The ascorbate is assumed to be filtered in the glomeruli and reabsorbed in the renal tubuli. The renal turnover suddenly increases at a certain plasma level (Figure 4), indicating a threshold value at which the tubular absorption is exceeded by the glomerular filtration. The renal... 

Normally, amino acids in the glomerular filtrate are reabsorbed in the proximal tubules. They may be present in urine in excessive amount because the plasma concentration exceeds the renal threshold. or because there is specific failure of normal tubularreabsorptivc mechanisms, such as in the inherited metabolic disorder, cystinuria, or more commonly because of acquired renal tubular damage. 

Prolongation of the 2-min half-life of native human GLP-1 was achieved through a rational analysis of the structure-activity relationship of numerous fatty acid-derivatized human GLP-1 analogues that showed resistance to DPPIV-mediated inactivation and avoided renal clearance through binding to albumin that exceeds the molecular threshold for glomerular filtration [11]. 

In contrast to what happens in plasma, the amino acid content of urine is increased. Increased amounts of j8-aminoisobutyric acid, ethylalanine, isoglutaric acid, taurine, and histidine have been reported. The increase results from reabsorption failure of the kidney, either because of renal damage or because the amount of amino acid in the glomerular filtrate exceeds tubular thresholds. Neither of these interpretations is quite satisfactory since there is usually no renal damage in kwashiorkor, and the amino acid level is reduced in plasma. 

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