Nephrotic syndrome patients with

Nephrotic syndrome. Patients with minimal change disease respond well to daily or alternate day therapy. With a total of prednisolone 60 mg/d, 90% of those who will lose their proteinuria will have done so within 4-6 weeks, and the dose is tapered off over 3-4 months. Longer courses only induce adverse effects. Relapses are common (50%) and it is then necessary to find a minimum dose of steroid that will keep the patient well. If a steroid is for any reason undesirable, cyclophosphamide or chlorambucil may be substituted. Membranous nephropathy may respond to high dose corticosteroid with or without chlorambucil. 

Membranous nephropathy is rare and causes the nephrotic syndrome, usually with minimal-change glomerulopathy, with or without interstitial nephritis (SEDA-11, 85). A retrospective study provided more data on the frequency and clinical characteristics of membranous nephropathy associated with NSAIDs (158). It confirmed that it is rare (13 of 125 patients diagnosed during the last 20 years met the strict criteria for NSAID-associated membranous nephropathy), and the nephrotic syndrome is reversible after prompt withdrawal. The pathogenesis is unknown but seems to be immune-mediated, given the characteristic deposition of IgG and C3. 

Sieberth HG, Clasen W, Fuhs M, IttelT, Kindler J, Mihatsch MJ. Serial kidney biopsies in patients with nephrotic syndrome treated with cyclosporin. J Autoimmun 1992 5 SuppI A 355-361. 

Nephrotic syndrome characteristic of excretion of protein in urine in excess of 2.5 g per day is not present in most patients with glomerulonephritis. These patients may present with a reduced glomerular filtration rate and varying degrees of proteinuria with or without hematuria, a condition referred to as the nephritic syndrome. Patients with nephritic syndrome may recover or worsen with chronic renal failure. 

The development of an acute interstitial inflammatory reaction in the kidney related to the administration of certain classes of drugs and leading to renal failure has been recognized for almost a century [42]. Antibiotics, in particular the sulfonamides [43] and semisynthetic penicillins [44, 45], were recognized as etio-logically associated in many instances. A retrospective review of 1068 kidney biopsies from 1%8 to 1997 by Schwarz et al. yielded acute interstitial nephritis in 6.5% of cases. In the majority of instances (85%) acute interstitial nephritis was drug related. Diuretics were implicated in 7.8 % of these cases [46]. Lyons et al. noted that four patients with proliferative glomerulonephritis and nephrotic syndrome treated with sulfonamide-derivative diuretics (furosemide or thiazides) developed severe renal failure, which reversed when the diuretic was withdrawn and prednisone was adminis-... 

In a 24-month prospective, randomised, open-label multicenter exploratory study on Chinese patients with biopsy-proven pure class V membranous lupus nephritis with nephrotic syndrome, patients were randomised to treatment with prednisolone plus either MMF or TAG. Adverse events in tiie MMF group included herpes zoster and reversible leucopenia, each in only one patient [29 ]. 

Loop diuretics are the drugs of choice for the treatment of edematous patients with congestive heart failure, cirrhosis of the liver, and nephrotic syndrome. Excretion of Na is helpful only to the extent that some of the... 

Loop diuretics are used in the treatment of edema associated with CHF, cirrhosis of the liver, and renal disease, including the nephrotic syndrome. These drug s are particularly useful when a greater diuretic effect is desired. Furosemide is the drug of choice when a rapid diuresis is needed or if the patient has renal insufficiency. Furosemide and torsemide are also used to treat hypertension. Ethacrynic acid is also used for the short-term management of ascites caused by a malignancy, idiopathic edema, or lymphedema. 

Plasma protein fractions are used to treat hypovolemic (low blood volume) shock that occurs as the result of bums, trauma, surgery, and infections, or in conditions where shock is not currently present but likely to occur. Plasma protein fractions are also used to treat hypoproteinemia (a deficiency of protein in the blood), as might be seen in patients with nephrotic syndrome and hepatic cirrhosis, as well as other diseases or disorders. As with human pooled plasma, blood type and crossmatch is not needed when plasma protein fractions are given. 

Clofibrate causes a necrotizing myopathy, particularly in patients with renal failure, nephrotic syndrome or hypothyroidism. The myopathy is painful and myokymia of unknown origin is sometimes present. The mechanism of damage is not known, but p-chlorophenol is a major metabolite of clofibrate and p-chlorophe-nol is a particularly potent uncoupler of cellular oxidative phosphorylation and disrupts the fluidity of lipid membranes. Muscle damage is repaired rapidly on the cessation of treatment. 

Hypotonic hyponatremia with an increase in ECF is also known as dilutional hyponatremia. In this scenario, patients have an excess of total body sodium and TBW however, the excess in TBW is greater than the excess in total body sodium. Common causes include CHF, hepatic cirrhosis, and nephrotic syndrome. Treatment includes sodium and fluid restriction in conjunction with treatment of the underlying disorder—for example, salt and water restrictions are used in the setting of CHF along with loop diuretics, angiotensin-converting enzyme inhibitors, and spironolactone.15... 

Edema can occur in patients with decreased myocardial contractility, nephrotic syndrome, or cirrhosis. 

Pure Hp was first isolated from the urine of a patient with the nephrotic syndrome (J7). Urines from other patients with this diagnosis have never proved suitable as a source for preparation of Hp. 

The author has observed a marked hypogammaglobulinemia in patients with the nephrotic syndrome in both the West Indies and Nigeria. In these patients the serum IgG level may be less than 500 mg/100 ml, and the urine electrophoretic pattern may resemble that of a normal serum. The striking hypogammaglobulinemia which so frequently accompanies chronic glomerular nephritis is responsible for the superimposed infection that may occur in this condition. 

Hypercholesterolaemia and hypertriglyceridaemia commonly occur in patients with severe proteinuria. It may be associated with a higher incidence of cardiovascular disease. Dietary treatment is of limited value if the underlying cause of the nephrotic syndrome is not successfully controlled. Statins should be considered to lower the serum cholesterol. 

The first point is that treatment with steroids is generally palliative rather than curative, and only in a very few diseases, such as leukemia and nephrotic syndrome, do corticosteroids alter prognosis. One must also consider which is worse, the disease to be treated or possible induced hypercortisolism. The patient s age can be an important factor, since such adverse effects as hypertension are more apt to occur in old and infirm individuals, especially in those with underlying cardiovascular disease. Glucocorticoids should be used with caution during pregnancy. If steroids are to be employed, prednisone or prednisolone should be used, since they cross the placenta poorly. 

Nephrotic syndrome may be noted in patients with history of renal disease. 

Rare reactions with long-term use include peptic ulcer disease, GI bleeding, gastritis, a severe hepatic reaction (cholestasis, jaundice), nephrotoxicity (dysuria, hematuria, proteinuria, nephrotic syndrome), and a severe hypersensitivity reaction (particularly in patients with systemic lupus erythematosus or other collagen diseases). 

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. 

Patients with nephrotic syndrome can lose vitamin D metabolites in the urine, presumably by loss of the vitamin D-binding protein. Such patients may have very low 25(OH)D levels. Some of them develop bone disease. It is not yet clear what value vitamin D therapy has in such patients, because therapeutic trials with vitamin D (or any other vitamin D metabolite) have not yet been carried out. Because the problem is not related to vitamin D metabolism, one would not anticipate any advantage in using the more expensive vitamin D metabolites in place of vitamin D itself. 

Prednisolone can cause an abrupt rise in proteinuria in patients with nephrotic syndrome. A placebo-controlled study in 26 patients aged 18-68 years with nephrotic syndrome has clarified the mechanisms responsible for this (163). Systemic and renal hemodynamics and urinary protein excretion were measured after prednisolone (125 mg or 150 mg when body weight exceeded 75 kg) and after placebo. Prednisolone increased proteinuria by changing the size-selective barrier of the glomerular capillaries. Neither the renin-angiotensin axis nor prostaglandins were involved in these effects of prednisolone on proteinuria. 

The author proposed that raised arterial pressure, which is an adverse effect of high dose glucocorticoid treatment, and low oncotic pressure due to a low protein plasma concentration in a patient with nephrotic syndrome, could have increased trans-synovial fluid flow at a lower arterial pressure than normal. 

Withdrawal symptoms disappear if the glucocorticoid is resumed, but as a rule they will in any case vanish spontaneously within a few days. More serious consequences can ensue, however, in certain types of cases and if adrenal cortical atrophy is severe. In patients treated with corticoids for the nephrotic syndrome and apparently cured, the syndrome is particularly likely to relapse on withdrawal of therapy if the adrenal cortex is atrophic (SEDA-3,305). In some cases, acute adrenocortical insufficiency after glucocorticoid treatment has actually proved fatal. It is advisable to withdraw long-term glucocorticoid therapy gradually so that the cortex has sufficient opportunity to recover. Table 5 lists methods of... 

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