Giuliano Colasanti

Idiopathic IgA mesangial nephropathy. Clinical and histological study of 374 patients.

Histological features and data on the natural history after 1 to 45 years (mean 6.56 +/- 8.55) of total apparent duration and 1 to 13 years (mean 3.48 +/- 5.04) of post-biopsy follow-up, are reported in 374 patients (mean age, 33.9 +/- 11.9 yrs) with idiopathic mesangial IgA nephropathy, who presented with a history of macroscopic hematuria (56%), recurrent in two-thirds of the patients, or with persistent microscopic hematuria and no previous episodes of gross hematuria (44%). Mesangial cell proliferation ranged from minimal to diffuse. Associated varying degrees of extracapillary proliferation, segmental and global glomerular sclerosis, tubulo-interstitial damage and arteriolar hyalinosis usually correlated with each other and with the extent of mesangial proliferation (P less than 0.05). The actuarial curve of progression to renal death showed a 75% survival after 20 years from apparent onset. Progression to renal failure was more rapid in patients with: an older age at onset (P = 0.0582); male sex (P = 0.0730); no history of recurrent gross hematuria (P = 0.0406); high blood pressure (P = 0.0011); more marked global (P = 0.0007) and segmental (P = 0.0026) glomerular sclerosis; more severe interstitial sclerosis (P = 0.0147); more diffuse and global mesangial proliferation (P = 0.0820); mesangio-parietal pattern at immunofluorescence (P = 0.0778). However, all these parameters showed a poor predictive value if applied to any single patient.

Characterization of interstitial infiltrating cells in Berger's disease.

The role of infiltrating blood-borne cells in the pathogenesis of renal damage in human glomerulonephritis is under active investigation. We have evaluated leukocyte infiltrates (number of cells/mm2) in the renal interstitium of 21 patients with Bergers disease and eight normal kidneys with monoclonal antibodies and a four-layer immunoperoxidase technique. In our population of patients, the number of infiltrating T-lymphocytes (OKT11+ cells) was significantly higher (median, 132) than in the normal kidneys (median, 60). This increase was mainly due to T-suppressor/cytotoxic lymphocytes (OKT8+ cells; median, 68), while T-helper/inducer lymphocytes (Leu 3A+ cells) and monocytes were in the normal range. T-lymphocyte infiltration was more marked in ten patients with impaired glomerular filtration rate (GFR) at the time of biopsy (median, 167) than in patients with normal GFR (median, 88). In addition, ten patients who showed deterioration of renal function during the subsequent follow-up, whatever their serum creatinine levels at the time of biopsy, had significantly more total T cells (median, 269), OKT8+ cells (median, 143), and Leu 3A+ cells (median, 105) than 11 patients with persistently stable GFR and normal controls. More data are necessary to establish whether this T-lymphocyte infiltration is the consequence of a cell-mediated mechanism acting in the interstitium, concomitant with the immune-complex-mediated mechanism acting in the glomerulus, or is a nonspecific consequence of the tubulointerstitial damage induced by the immunologically mediated glomerular disease.

Histological and immunohistological features in essential mixed cryoglobulinemia glomerulonephritis

The glomerulonephritis (GN) of essential mixed cryoglobulinemia (EMC) shows some characteristic histological lesions which differentiate the renal involvement in this form from the glomerular lesions found in various types of idiopathic or systemic GN.

Lymphocyte Populations in the Peripheral Blood from Patients with IgA Nephropathy

On the basis of a reported increase of circulating surface IgA-bearing lymphocytes in Japanese patients with IgA nephropathy, peripheral blood lymphocyte populations have been studied in 22 Italian pa

Prognostic factors in essential mixed cryoglobulinemia nephropathy

Kidney involvement in Essential Mixed Cryoglobulinemia (EMC) varies from 8 to 58% in the large series of patients [1–3] and is often regarded as an ominous prognostic sign [4]. We report here the outcome of 116 patients with EMC nephritis.

Some aspects of kidney involvement in plasma cell dyscrasias: A forum

SOLOMON: The first point for the nephrologists is to maintain a high level of suspicion. In other words, in a patient with unexplained proteinuria or some manifestation of renal dysfunction it is necessary for the clinician to keep the possibility in mind that this patient may have a some type of light chain related renal disease. This is very often overlooked. Secondly, I would like to reiterate the importance of recognizing the presence of Bence Jones proteinuria, especially in patients with nephrotic syndrome. Immunofixation on urine concentrated 50–100 fold is the preferable method of analysis. In a patient with nephrotic syndrome there is so much serum protein in the urine (especially transferrin, albumin, etc.), that the monoclonal light chain component is often very difficult to detect. Not infrequently the diagnosis of amyloidosis responsible for the nephrotic syndrome is not made until a renal biopsy is done. In retrospect a careful analysis of the urine using serological techniques will disclose the presence of Bence Jones protein. The antisera that the hospital laboratory uses is also very important. Many of the commercial anti-light chain antisera are not very satisfactory (particularly for the detection of lambda chains). For example, to detect the lambda VI Bence Jones proteins requires a special antiserum; this antiserum is not commercially available as yet, however the identification of Bence Jones proteins of this subgroup indicates with high probability amyloidosis.

The Glomerulonephritis of Essential Mixed Cryoglobulinemia

In cryoglobulinemia there are immunoglobulins in the blood that precipitate reversibly in the cold. The most widely accepted classification, recognizes three types of cryoglobulinemia [1]. In type I cryoglobulinemia, the cryoprecipitable Ig is a single monoclonal Ig, usually a myeloma protein or a macroglobulin. Type II and type III are mixed cryoglobulinemias, containing a polyclonal IgG and an anti-IgG rheumatoid factor, most frequently of the IgM class. The IgM antiglobulin component in type III cryoglobulinemia is polyclonal, is probably antigen-driven and seems to be result of an abnormal overactivity of physiological immunoregulatory mechanisms. On the contrary, the IgM antiglobulin component in type II cryoglobulinemia is monoclonal, and since it is due to abnormal proliferation of a special clone of B lymphocytes, it probably is the consequence of a plasma cell dyscrasia

The Role of Renal Biopsy in Acute Renal Failure

There is agreement among the nephrologists that renal biopsy is of value for selected patients with acute uremia. It may be indicated for making or confirming a clinical diagnosis, to assess prognosis or to provide a basis for treatment.

Plasma-exchange in immunologically mediated glomerular diseases

SummaryIntensive plasma-exchange, usually combined with steroids and cyclophosphamide, was carried out in 10 patients with rapidly progressive crescentic glomerulonephritis (primary in six and associated with systemic diseases in four), and in 11 adult patients with severe non-crescentic glomerulonephritis associated with systemic lupus erythematosus in four, and with essential mixed cryoglobulinemia in seven. Therapeutic benefit with improvement in renal function, possibly due to the effect of PE, was achieved in 8/10 patients with RPCGN, in 3/4 patients with SLE non-crescentic nephritis and in 6/7 patients with EMC nephritis.