Kidney nephrotic syndrome

The physiology of amyloid pleural effusions is complex. AL amyloidosis can alter the function of several organs that could contribute to effusion formation including the heart (infiltrative cardiomyopathy—48% cases), kidneys (nephrotic syndrome—65% cases), and thyroid (hypothyroidism—4% cases) (20). 

These studies led to the realization that proteinuria— the abnormal appearance of protein in the urine— could result not only from the enlargement of submicroscopic holes in the glomerular capillary wall, but also from the loss or neutralization of its negatively charged components. This finding has provided a new direction for research on the molecular basis for the nephrotic syndrome, a group of kidney diseases all characterized by massive proteinuria. 

Inherited defects in lipoprotein metabofism lead to the primary condition of either hypo- or hyperlipoproteinemia (Table 26-1). In addition, diseases such as diabetes mellitus, hypothyroidism, kidney disease (nephrotic syndrome), and atherosclerosis are associated with secondary abnormal hpoprotein patterns that are very similar to one or another of the primary inherited conditions. Virtually all of the primary conditions are due to a defect at a stage in hpoprotein formation, transport, or destruction (see Figures 25—, 26-5, and 26-6). Not all of the abnormafities are harmful. 

Albumin 18-20 Maintains plasma oncotic pressure transports small molecules Dehydration, anabolic steroids, insulin, infection Overhydration, edema, kidney insufficiency, nephrotic syndrome, poor dietary intake, impaired digestion, burns, congestive heart failure, cirrhosis, thyro id/adrena / pitu itary hormones, trauma, sepsis... 

Kidney Tubular cells Low MW proteins (Lysozyme) Rat, man Nephrotic syndrome Renal cancer... 

Bumetanide is used for relieving edema associated with cardiac insufficiency, for liver and kidney diseases including nephrotic syndrome, for ascites, and hypertension. Synonyms of this drug are bumex and others. 

Patients with renal diseases leading to the nephrotic syndrome often present complex problems in volume management. These patients may exhibit fluid retention in the form of ascites or edema but have reduced plasma volume due to reduced plasma oncotic pressures. This is very often the case in patients with "minimal change" nephropathy. In these patients, diuretic use may cause further reductions in plasma volume that can impair GFR and may lead to orthostatic hypotension. Most other causes of nephrotic syndrome are associated with primary retention of salt and water by the kidney, leading to expanded plasma volume and hypertension despite the low plasma oncotic pressure. In these cases, diuretic therapy may be beneficial in controlling the volume-dependent component of hypertension. 

Yoshioka K, Ohashi Y, Sakai T, Ito H, Yoshikawa N, Nakamura H, Tanizawa T, Wada H, Maki S. A multicenter trial of mizoribine compared with placebo in children with frequently relapsing nephrotic syndrome. Kidney Int 2000 58(l) 317-24. 

Aspirin and similar NSAIDs can cause other toxic side effects if used improperly or if taken by patients who have preexisting diseases. For instance, serious hepato-toxicity is rare with normal therapeutic use, but high doses of aspirinlike drugs can produce adverse changes in hepatic function in patients with liver disease.85,99 Likewise, aspirin does not seem to cause renal disease in an individual with normal kidneys,84 but problems such as nephrotic syndrome, acute interstitial nephritis, and even acute renal failure have been observed when aspirin is given to patients with impaired renal function, or people with decreased body water (volume depletion).35,102... 

Cyclosporine Neoral, Sandimmune Kidney, liver, heart, lung, pancreas, bone marrow Psoriasis, rheumatoid arthritis, nephrotic syndrome... 

Nephrotic syndrome. Thiazide or loop diuretics are used in the treatment of this kidney disorder that causes increased protein in the urine. 

Loop diuretics induce renal prostaglandin synthesis, and these prostaglandins participate in the renal actions of these drugs. NSAIDs (eg, indomethacin) can interfere with the actions of the loop diuretics by reducing prostaglandin synthesis in the kidney. This interference is minimal in otherwise normal subjects but may be significant in patients with nephrotic syndrome or hepatic cirrhosis. 

The concomitant administration of ibuprofen antagonizes the irreversible platelet inhibition induced by aspirin. Thus, treatment with ibuprofen in patients with increased cardiovascular risk may limit the cardioprotective effects of aspirin. Rare hematologic effects include agranulocytosis and aplastic anemia. Effects on the kidney (as with all NSAIDs) include acute renal failure, interstitial nephritis, and nephrotic syndrome, but these occur very rarely. Finally, hepatitis has been reported. 

Because the sulfide may be reoxidized to the inactive prodrug in the kidney, sulindac may inhibit renal COX less than other NSAIDs, though reversible renal failure and nephrotic syndrome have been observed with this drug. Among the more severe reactions, Stevens-Johnson epidermal necrolysis syndrome, thrombocytopenia, agranulocytosis, and nephrotic syndrome have all been observed. Like diclofenac, sulindac may have some propensity to cause elevation of serum aminotransferases it is also sometimes associated with cholestatic liver damage, which disappears or becomes quiescent when the drug is stopped. 

Minimal change disease is the most common cause of nephrotic syndrome in children, presenting typically with rapid onset of mostly steroid-sensitive nephrotic syndrome, usually with selective proteinuria (albuminuria). Light-microscopic morphology of the kidney is normal and immunofluorescence is negative. Foot process effacement on electron microscopy is the only observed pathology. 

B6. Bergrem, H., Pharmacokinetics and protein binding of prednisolone in patients with nephrotic syndrome and patients undergoing hemodialysis. Kidney Int. 23, 876-881 (1983). 

D3. Dantal, J., Bigot, E., Bogers, W., Testa, A., Kriaa, F., Jacques, Y., Hurault de Ligny, B., Niaudet, P., Charpentier, B., and Soulillou, J. P., Effect of plasma protein adsorption on protein excretion in kidney-transplant recipients with recurrent nephrotic syndrome. N. Engl. J. Med. 330, 7-14 (1994). 

G7. Grausz, H., Lieberman, R., and Earley, L. E., Effect of plasma albumin on sodium reabsorption in patients with nephrotic syndrome. Kidney Int. 1, 47-54 (1972). 

LI. Laine,J.,Jalanko, H., Holthofer,H.,Krogerus,L., Rapola,J., vonWillebrand,E.,Lautenschlager, I., Salmela, K., and Holmberg, C., Post-transplantation nephrosis in congenital nephrotic syndrome of the Finnish type. Kidney Int. 44, 867-874 (1993). 

Ordonez, J. D., Hiatt, R. A., Killebrew, E. J., and Fireman, B. H., The increased risk of coronary heart disease associated with nephrotic syndrome. Kidney Int. 44, 638-642 (1993). 

P7. Peterson, C., Madsen, B., Perlman, A., Chan, A. Y., and Myers, B. D., Atrial natriuretic peptide and the renal response to hypervolemia in nephrotic humans. Kidney Int. 34, 825—831 (1988). P8. Plum, J., Mirzaian, Y., and Grabensee, B., Atrial natriuretic peptide, sodium retention, and proteinuria in nephrotic syndrome. Nephrol. Dial. Transplant. 11, 1034—1042 (1996). 

Schnaper, H. W., A regulatory system for soluble immune response suppressor production in steroid-responsive nephrotic syndrome. Kidney Int. 38, 151-159 (1990). 

In 54 patients, a kidney biopsy was performed 13.2 8.9 days after onset (n = 32). In all patients, the findings suggested either acute tubular necrosis or its recovery phase. The underlying diseases included kidney diseases such as IgA nephropathy [138], minimal change nephrotic syndrome [139], autosomal dominant polycystic kidney disease (ADPKD) [140], and cystinuria [67]. 

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