[Xerostomia and Xerophthalmia in haemodialysis patients]. / Xerostomia e Xeroftalmia nei pazienti in dialisi.

BACKGROUND: A reduction in salivary and lachrymal secretion has been described in many pathologies; however, such alterations have not been described in patients with renal failure. This study was designed to estimate the frequency of alterations in salivary and lachrymal secretion in haemodialysed patients. PATIENTS ABD METHODS: We studied 63 haemodialysed patients and 23 healthy control subjects. In all of them we tested salivary secretion (Saxon test), lachrymal secretion (Shirmer test) as well as the presence of symptoms of xerostomia and xerophthalmia. In a subgroup of patients We investigated any evidence of ocular lesions and tissue damage of salivary glands (histopathology). We also tested the correlation between salivary and lachrymal secretion and autonomic nervous system function. Furthermore, we also studied the association between xerostomia and xerophthalmia and serum auto antibodies (anti nuclear, anti-Ro (SS-A), anti-La (SS-B)) and anti HCV antibodies. RESULTS: On average salivary and the lachrymal secretion was markedly reduced in uraemic patients compared with healthy controls. We found the alterations in salivary glands function to be strongly related to salivary glands fibrosis and atrophy and independent of amyloid accumulation. On the other hand, we observed that xerostomia and xerophthalmia were unrelated to autonomic dysfunction as well as to HCV infection and circulating auto antibodies. Moreover, xerophthalmia was frequently associated with evidence of corneal damage. CONCLUSIONS: Reduced salivary and lachrymal secretion is frequent in uraemic patients. Such alterations are often asymptomatic and could be an expression of the accelerated age-dependent decline in glandular function and the attendant fibrosis and atrophy.

The deletion polymorphism of the angiotensin-converting enzyme is associated with nephroangiosclerosis.

The D allele of the angiotensin-converting enzyme (ACE) gene has been linked with diabetic nephropathy and IgA glomerulonephritis and with faster renal disease progression. The association of this allele with nephroangiosclerosis has been scarcely investigated. We have tested this association in 45 hypertensive patients (all whites) with well defined nephroangiosclerosis (diagnosis established on the basis of renal biopsy in all cases) and moderate to severe renal failure. As studies of genetic association of small size often produce conflicting results, besides a control group of 343 Italian patients with essential hypertension and normal renal function, we elected to use also a very large control group of race-matched subjects taken from a meta-analysis of 27,565 whites. The proportion of patients with the D allele (64%) was higher in patients with nephroangiosclerosis than that in Italian hypertensives (54%) and in whites (54%). DD and DI genotypes were more prevalent in patients than in control groups. The dominant model (DD and DI v II: nephroangiosclerosis v Italian controls: chi2 = 6.19, P = .012; nephroangiosclerosis v whites chi2 = 6.86, P = .009) fitted the data better than the codominant and the recessive model (P < or = .022). The D allele is associated with nephroangiosclerosis with a dominant effect in the sample of patients studied. Although intervention studies are needed to see whether these findings imply a causal association, our data suggest that this allele may at least act as disease marker in nephroangiosclerosis.

Acute interstitial nephritis associated with uveitis and primary hypoparathyroidism.

In a study of a patient with acute renal failure and uveitis, renal biopsy showed acute interstitial nephritis. Serum calcium and parathyroid hormone concentrations were persistently low during the acute phase and after the resolution of renal failure. Clinical history was negative for intake of drugs capable of inducing acute interstitial nephritis.

[Deposits with anti-globulin activity in dermatitis herpetiformis]. / Depositi con attività antiglobulinica nella dermatite erpetiforme.

Skin biopsy specimens from 2 patients with dermatitis herpetiformis were examined by means of direct immunofluorescence with fluoresceinated aggregated human IgG (FAIgG) for the presence of tissue antiglobulin activity. Positive FAIgG staining was seen in both skin biopsy specimens yielding a fluorescence pattern similar to that of immunoglobulin and complement deposits. Tissue antiglobulin activity was no more detectable in a second skin biopsy obtained from one patient whose rash was controlled by Dapsone. These findings suggest an involvement of tissue antiglobulin activity in the pathogenesis of dermatitis herpetiformis. In fact, tissue antiglobulin activity is capable of acting as an immunoabsorbent and binding immunocomplexes from the circulation.

The 'breakpoint' test, a new statistical method for studying progression of chronic renal failure.

The application of a new statistical method ('breakpoint' test) to the study of the progression of chronic renal failure is described. This test establishes whether the best fit of a series of GFR measurements is linear or broken. Such an approach avoids the analytical constraint of the time of intervention assumed by other methods. Re-analysis by this test of previous studies of low-protein diet suggests that in some cases the effect of the dietary regimen has been overemphasized.

Glomerular deposits of rheumatoid factor in glomerulonephritis.

One hundred and forty-four kidney biopsy specimens with various forms of glomerulonephritis were studied to assess the presence of Rheumatoid Factor (RF) deposits. RF deposits were found in 21 specimens: six with acute post-streptococcal glomerulonephritis, two with crescentic glomerulonephritis, four with lupus nephritis, eight with essential mixed cryoglobulinaemia glomerulonephritis, and one with end-stage kidney disease. Blocking and elution studies carried out on specimens with essential mixed cryoglobulinaemia provided evidence that the RF deposits derive from circulating monoclonal RF. This data suggests that RF participates in the formation of glomerular immune deposits in several forms of immune complex mediated glomerulonephritis.

Glomerular localization of circulating antiglobulin activity in essential mixed cryoglobulinemia with glomerulonephritis.

Kidney biopsy samples from 27 patients with essential mixed cryoglobulinemia of the IgG-IgM(k) type and glomerulonephritis were studied to assess whether glomerular immunodeposits display antiglobulin (AG) activity similar to that of serum cryo-IgM. A preparation of heat-aggregated human IgG (FAIgG) was used to search for tissue AG activity, and blocking tests and reactivity tests were carried out to define the nature of this activity. Glomerular localization of FAIgG was observed in 17 out of 27 kidney specimens, the positive findings being always associated with IgM deposits. Prior exposure of tissue sections to anti-IgM serum blocked the FAIgG reaction, but no such effect was produced by the pretreatment with other antisera. The positive FAIgG tissue specimens yielded a similar fluorescence pattern with aggregated alkylated-reduced IgG, but did not react at all with the aggregated F(ab')2 or aggregated albumin. The IgM recovered in the eluate of a kidney biopsy specimen displayed AG activity. Patients with AG deposits showed more severe histologic changes and a greater renal functional impairment than did those without. The data support the notion that circulating cryo-IgM anti-IgG participates in the formation of glomerular immunodeposits and in the genesis of renal damage.

HBsAg immune complex glomerulonephritis.

Out of 97 patients with various forms of glomerulonephritis 10 were found to be HBsAg seropositive. None of these showed HBsAg immunodeposits within the kidney. Direct immunofluorescent kidney staining for HBsAg was observed in 4 out of 87 HBsAg seronegative patients. The HBsAg staining in kidneys was a false positive reaction due to binding of the Fc portion of the fluoresceinated IgG molecules to the IgM RF tissue deposits. The false positive reaction for HBsAg is not revealed by the usual specificity controls for fluorescence staining. The role of HBsAg in glomerulonephritis remains unproven.