Gerhard Treser

Nephropathy Induced by D-Penicillamine

Abstract Two patients given D-penicillamine for rheumatoid arthritis and scleroderma developed renal damage. In one patient, a renal biopsy had been obtained before treatment was begun that permitt...

Routine Immunohistology in Renal Diseases

Excerpt In 1907 it was suggested (1) that certain renal diseases may be caused by an immune reaction involving the glomerulus. This hypothesis has recently received renewed support. In 1951 we demo...

Occurrence and Nature of Glomerular Lesions after Group A Streptococci Infections in Children

Abstract A prospective study of renal involvement after group A streptococci infections was undertaken in 248 children who had weekly examinations for at least 6 weeks. Examination included urinaly...

Hyponatremia in patients with the acquired immunodeficiency syndrome

Of 103 patients with the acquired immunodeficiency syndrome (AIDS) admitted for acute opportunistic infections, 36 had serum sodium less than or equal to 130 mEq/l (130 mmol/l). In 12 the hyponatremia was associated with volume depletion and corrected with saline replacement therapy. In 23 it was associated with the syndrome of inappropriate antidiuretic hormones secretion (SIADH). One patient had adrenal insufficiency and the serum sodium corrected after steroid replacement. We conclude that hyponatremia is a common electrolyte abnormality in AIDS patients suffering acutely from opportunistic infections and that SIADH and volume depletion are important contributing factors.

Renal cytomembranous inclusions in idiopathic renal disease as predictive markers for the acquired immunodeficiency syndrome

Tubuloreticular inclusions (TRI) and cylindrical confronting cisternae (CCC) are present in cells of patients with the acquired immunodeficiency syndrome (AIDS) and have also been detected in the kidneys of individuals with AIDS and heavy proteinuria. We examined renal biopsy tissue from 13 patients with proteinuria and/or renal insufficiency. At the time of biopsy, two of the patients had AIDS (group A), four had AIDS-related complex (ARC) (group B), and seven presented without any clinical signs or symptoms characteristic of AIDS or ARC. These seven had risk factors for AIDS, and systemic lupus erythematosus (SLE) was excluded in all. Abundant TRI were present in the renal endothelial and fibroblastic interstitial cells in all patients from group A and B and in four patients who had no evidence for AIDS or ARC at the time of biopsy (group C). These individuals were followed, and all developed AIDS within a period of 3 to 14 months. CCC were detected in two of two patients in group A, one of four in group B, and one of four in group C. TRI and CCC were not present in the renal tissue of the remaining three patients; they did not develop ARC or AIDS over a prolonged observation period. Our findings suggest that TRI and TRF are ultrastructural markers for human immunodeficiency virus (HIV) associated nephropathy and can be seen before AIDS has manifested itself. These structures may be of predictive value for the future development of AIDS in patients presenting with apparent idiopathic renal disease.

Glomerular lesions in a strain of genetically diabetic mice.

Summary In a strain of genetically determined, spontaneously diabetic mice (KK mice) lesions similar to those seen in human diabetic nephropathy were found in the glomeruli. These lesions increased with age and consisted of diffuse and nodular mesangial changes, exudative lesions, and alterations of the basement membranes.

Circulating Immune Complexes in Patients with Uncomplicated Group A Streptococcal Pharyngitis and Patients with Acute Poststreptococcal Glomerulonephritis

To investigate the role of circulating immune complexes (CIC) in the pathogenesis of acute poststreptococcal glomerulonephritis (AGN), sera were obtained serially from 13 patients with biopsy-proven AGN, 16 patients with group A streptococcal infection, and 20 age- and sex-matched controls. Samples were analysed for Clq-binding activity (Clq-BA), levels of IgG, IgA, IgM, C3 and C4, and antibody titres to streptococcal enzymes. Significant elevation of Clq-BA was observed in 11 patients (84.5%) with AGN and 7 patients (44%) with streptococcal infection alone. The data suggest that CIC do not necessarily cause glomerular damage, but rather represent a systemic inflammatory response in patients with group A streptococcal infection.

SPECIFICITY OF IMMUNOFLUORESCENCE IN EXPERIMENTAL AND HUMAN RENAL DISEASES.

Summary Severe proteinuria with considerable gamma globulin content was produced in rats by aminonucleoside injections. Sections of their kidneys at intervals between 4 and 12 days after onset of proteinuria did not show immunofluorescent staining for gamma globulin and complement. Rats made nephritic by injection of anti-rat kidney rabbit serum showed immediate morphologic damage and proteinuria with considerable gamma globulin content. Rabbit gamma globulin can be demonstrated immediately on the glomeruli while rat gamma globulin does not appear before the seventh day of disease. A kidney biopsy of a patient with multiple myeloma and advanced renal damage did not show immune staining for gamma globulin and complement, in spite of a severe proteinuria with large amounts of albumin, Bence-Jones protein and gamma globulin in the urine. Positive immune staining for gamma globulin or complement and its components in renal diseases can therefore not be attributed to trapping or unspecific transudation in the damaged kidney.

IgA nephropathy occurring in the context of previous acute glomerulonephritis.

A 37-year-old female presented with acute onset of glomerulonephritis 10 days following an upper respiratory infection. Serum complement components were depressed and proteinuria exceeded 3.0 g daily. Renal biopsy revealed granular staining of IgG and C3 along the basement membrane as well as small amounts of IgA in a linear pattern. Gradual resolution of symptoms was followed by recrudescent proteinuria 2 years later. Renal biopsy at this time revealed large deposits of IgA in a mesangial staining pattern consistent with a diagnosis of IgA nephropathy. Possible mechanisms for this unusual morphologic transformation include enhanced mesangial permeability as well as mesangial sequestration of an exogenous antigen.

Pathology of Human Immunodeficiency Virus (HIV) Associated Nephropathy in Adults and Children

A variety of renal lesions are identified in patients infected with Human Immunodeficiency virus (HIV). A distinctive clinicopathologic entity, termed HIV-associated nephropathy (HIVAN) is noted in 7–10% of the unselected adult and pediatric hospital admissions for Acquired Immunodeficiency Syndrome (AIDS). Adult HIVAN is more common in Blacks and in intravenous (IV) drug users and is characterized clinically by acute onset of severe, often nephrotic range proteinuria with generally rapid and irreversible progression to renal failure. Histologically, focal segmental sclerosis (FGS) is frequently accompanied by a unique globally collapsing glomerulopathy with dilatation of Bowman’s space, microcystic ectasia of tubules, scant interstitial cellular infiltrate and fibrosis in the well established lesions. A combination of these distinctive clinical features and histologic findings, along with abundant tubulo-reticular inclusions (TRI) in renal vascular endothelium on electronmicroscopy, distinguishes HIVAN from heroin-associated nephropathy (HAN). A constellation of these clinicopathological findings also allows one to make a presumptive diagnosis of HIV infection with a high degree of accuracy in an asymptomatic HIV carrier. Greater frequency of multiple, budding, and complex nuclear bodies, and various cytomembranous and intranuclear inclusions, presumed to be “viral footprints,” suggest a viral etiology for HIVAN.