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Tubular diseases

In some human studies where clinical chemistry measurements but no renal biopsies were performed, the only parameter of renal function shown to be affected was an increase in the levels of NAG in the urine. NAG is a lysosomal enzyme present in renal tubular cells that has been shown to be a sensitive indicator of early subclinical renal tubular disease. The mechanism by which lead affects the release of NAG from renal tubular cells is not known, but it is suggested that lead could attach to kidney cell membranes and alter membrane permeability (Chia et al. 1994). [Pg.267]

Chronic renal failure is characterized by progressive azotemia over weeks and months. It may be a consequence of many primary glomerulonephritic and tubular diseases. The urine abnormalities are dependent upon the underlying disease, although isosthenuria is common when CRF is advanced. Hypertension develops in the majority of patients. [Pg.611]

Kidney disease Upper respiratory tract infection Urinary tract infections Amyloidosis Tubular disease Glomerulonephritis... [Pg.236]

A decrease in the PAH clearance might be due to either an actual dechne in renal plasma flow or a decrease in the extraction factor of PAH. The latter occurs when the tubular secretion of PAH in proximal tubules is impaired due to tubular disease or the presence of substances, which compete with transceUular... [Pg.100]

Diseases of the kidney that are discussed in this section include (1) the uremic syndrome, (2) chronic kidney disease, (3) end-stage renal disease, (4) diabetic nephropathy, (5) hypertensive nephropathy, (6) glomerular diseases, (7) interstitial nephritis, (8) polycystic Iddney disease, (9) polycystic kidney disease, (10) toxic nephropathy, (11) obstructive uropathy, (12) tubular diseases, (13) renal calculi, and (14) cystinuria. In addition, this section also includes discussions on (1) prostaglandins and NS AIDS in kidney disease, (2) monoclonal light chains and kidney disease, and (3) urinary osmolality. [Pg.1691]

Types of tubular disease discussed in this section include renal tubular acidoses and inherited tubulopathies. [Pg.1707]

HCO3. Hyperchloremic acidosis maybe a sign of severe renal tubular disease. [Pg.1757]

While previous studies have focused on MPO in cardiovascular disease, it is important to consider the role of monocytes, macrophages, eosinophils, and neutrophils as mediators of innate immunity, and as important responsive cells in inflammation. The role of MPO and EPO and their hypohalous acids targeting lipids to generate novel halogenated lipids is relatively unexplored, and should be thoroughly examined, in diseases including pancreatitis, asthma, renal glomerular, and tubular disease. [Pg.82]

The effect of pyrazinamide on urate excretion was determined by measurement of urate excretion during 3 consecutive 20-minute urine collection periods beginning one hour after the oral administration of 3g of pyrazinamide. The collection period with the lowest excretion of uric acid was considered to represent maximum suppression of uric acid excretion. Urate excretion decreased from a mean of 372 38 agm/min during control periods to 27 4 igm/min after pyrazinamide (Table 2). The decrease in urate excretion which follows pyrazinamide administration has generally been considered to provide an estimate of urate secretion. Post-pyrazinamide urate excretion was 7.3 2% of baseline excretion in the 16 sickle cell anemia patients compared to 16.8 2.9% in 12 normal subjects (p <. 01). Thus, the present findings are consistent with increased urate secretion in sickle cell anemia. Since all of the patients studied had renal tubular disease, at least as indicated by inability to concentrate their urine normally, impaired post-secretory urate reabsoirption is a more probable interpretation of these results than enhanced secretion. [Pg.374]

Asherson RA, Cervera R, Piette J-C, Schoenfeld Y (1996) The antiphospholipid syndrome. CRC Press, Boca Raton Avni EE Robberecht MS, Lebrun D et al (1983) Transient acute tubular disease in the newborn characteristic ultrasound pattern. Ann Radiol 26 175-182 Babcock DS (1989) Neonatal and pediatric ultrasonography. [Pg.379]


See other pages where Tubular diseases is mentioned: [Pg.286]    [Pg.258]    [Pg.249]    [Pg.120]    [Pg.102]    [Pg.109]    [Pg.31]    [Pg.376]    [Pg.249]    [Pg.1680]    [Pg.1707]    [Pg.2102]    [Pg.2103]    [Pg.632]    [Pg.634]    [Pg.638]    [Pg.87]    [Pg.1031]    [Pg.342]    [Pg.343]    [Pg.160]   
See also in sourсe #XX -- [ Pg.1707 , Pg.1708 , Pg.1709 , Pg.1710 ]




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