Nephrotic syndrome infection

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. 

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... 

Transferrin 8-9 Binds iron in plasma and transports iron to bone Iron deficiency, pregnancy, hypoxia, chronic blood loss, estrogens Chronic infection, cirrhosis, burns, enteropathies, nephrotic syndrome, cortisone, testosterone... 

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. 

Cerebral infarction has also been reported in association with the use of desmopressin in children (31,32). One of these cases involved a 7-month-old child with congenital nephrotic syndrome who developed a cerebral infarction after surgery (31). One child developed cerebral ischemia after Varicella infection and desmopressin for enuresis (32). 

Nephrotic syndrome is a life-threatening disease. Adult patients may die of thromboembolic complications and children may die of infections, and persistent nephrotic syndrome confers a substantial risk of progression to end-stage renal failure. 

Nephrotic patients (especially children) are prone to bacterial infections. Before antibiotics and corticosteroids were introduced into the therapy, pneumonia, peritonitis, and sepsis (usually caused by pneumococci) were the most frequent cause of death of nephrotic children with minimal change disease. Infections are more frequent in nephrotic children and after the age of 20 their prevalence markedly decreases because the majority of adults have antibodies against the capsular antigens of pneumococci. Infections remain an important complication of nephrotic syndrome in developing countries. In developed countries, nephrotic patients treated by immunosuppressive agents may frequently suffer from viral infections (mainly herpesvirus infections, e.g., cytomegalovirus and Epstein-Barr virus infections). 

The presence of edema and increased skin fragility (often the site of entrance of bacteria) are among the causes of increased risk of infections in nephrotic syndrome. Losses of immunoglobulin G and factor B (from the alternative pathway of the activation of complement) into the urine weaken the ability of the defense system to respond mainly to encapsulated microbes like pneumococci. The function of lymphocytes can be further weakened as a consequence of losses of zinc and transferrin into the urine. Weakening of the phagocytic function of macrophages has been described as well. 

Fig. 11. Cluster analysis used to assist in diagnosis of kidney diseases (adapted from Batchelor 418>). (A) acute nephritis, (B) nephrotic syndrome, (C) normal, (D) acute renal infection, (E) essential hypertension, and (F) chronic renal failure...

I.6. Various Diseases. Abbassy et al. (Al) observed in 12 cases of malnutrition (including kwashiorkor), toxic dyspepsia, 8 cases of acute nephritis, 8 cases of infective hepatitis, and muscular dystrophy an increased spontaneous excretion of xanthurenic acid, the amount of which was found to depend on the severity of the case. In all these cases, with the exception of acute nephritis and hepatitis, the amount of xanthurenic acid was restored to normal levels after vitamin Be therapy. In 8 children with mental retardation, cerebral palsy, recurrent convulsions, 5 with nephrotic syndrome, and 5 with pellagra the amount of xanthurenic acid spontaneously excreted was found to be within the normal range, indicating that pyridoxine is probably not concerned in these cases. 

Zikos, D., Grewal, K.S., Craig, K., Jen-CMeh-Cheng, Peterson, D.R., Fisher, K.A. Nephrotic syndrome and acute renal failure associated with hepatitis A virus infection. Amer. J. Gastroenterol. 1995 90 295-298... 

One renal transplant recipient developed the nephrotic syndrome, with microscopic hematuria and non-ohguric acute renal insufficiency within 15 days after starting foscarnet therapy for cytomegalovirus infection (13). A kidney biopsy showed crystals in aU glomeruh and in the proximal tubules. The crystals consisted of several forms of foscarnet salts. Renal function and proteinuria nevertheless improved progressively, and a second transplant biopsy 8 months after the first one showed... 

Kimmel PL, Ferreira-Centeno A, Farkas-SzallasiT, Abraham AA, Garrett CT. Viral DNAin microdissected renal biopsy material from HIV infected patients with the nephrotic syndrome. Kidney Int 1993 43 1347-1352. 

Despite a good overall safety profile, anti-TNF antibodies can induce a number of adverse effects, including autoimmunity and infections. A trial in the treatment of Crohn s disease noted infusion reactions, transient increased of anti-dsDNA antibodies, and serum sickness-like delayed hypersensitivity with retreatment. Induction of human-antichimeric-antibodies was suggested as the cause of some of the infusion reactions [90]. A prospective study in 35 patients with Crohn s disease showed induction of ANA and anti-dsDNA autoantibodies in 53% and 35% of infliximab-treated patients [91]. A single patient showed clinical features consistent with drug-induced lupus, including the presence of ANA and anti-dsDNA autoantibodies, which quickly resolved after discontinuation of infliximab. Reports on renal adverse effects of anti-TNF antibodies are very rare. Saint Marcoux described the occurrence of crescentic GN in as few as 2 patients out of a cohort of 39 patients, treated with an anti-TNF antibody for rheumatoid arthritis [92]. A case report by Chin et al. [93] described the case of a 29-year-old Australia-born Vietnamese who presented with nephrotic syndrome. A renal biopsy showed membranous nephropathy. Symptoms attenuated after discontinuation of infliximab therapy. 

AA protein is often deposited in chronic inflammatory diseases such as rheumatoid arthritis (incidence up to 20%) and other inflammatory joint diseases, and in chronic suppurative and granulomatous infections such as tuberculosis and osteomyelitis. Deposits of AA protein are also observed in nonlymphoid tumors such as renal and gastric carcinomas and in Hodgkin s disease. Deposits of AA protein are most often found in the kidneys, liver, and spleen, usually resulting in nephrotic syndrome and hepatosplenomegaly. 

Most patients present initially with edema, frequently acute in onset, following a nonspecific upper respiratory tract infection, allergic reaction, or vaccinations, which might have activated the T lymphocytes. Nephrotic syndrome with massive proteinuria (substantially more than 40 mg/m per hour for children and 3 g/day for adults), edema, hypoalbuminemia, and hyperlipidemia is common. The patient s weight may be increased dramatically because of sodium and fluid retention. Nephrotic features such as gross hematuria are uncommon. However, microscopic hematuria may be seen in up to 20% to 25% of patients. Hypertension and decreased renal function are uncommon in children but are more common in older adults. In some patients, volume depletion may result in mild to moderate azotemia. 

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