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Here, we report the occurrence of leukocytoclastic vasculitis as an outcome of type III allergy to insulin in a patient with type II diabetes mellitus. The diagnosis was made on the basis of anatomo-pathological examination of a skin biopsy.

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OBJECTIVE: The aim of this study was to investigate if low-level laser therapy (LLLT) can modulate formation of hemorrhagic lesions induced by immune complex. BACKGROUND DATA: There is a lack of information on LLLT effects in hemorrhagic injuries of high perfusion organs, and the relative efficacy of LLLT compared to anti-inflammatory drugs. METHODS: A controlled animal study was undertaken with 49 male Wistar rats randomly divided into seven groups. Bovine serum albumin (BSA) i.v. was injected through the trachea to induce an immune complex lung injury. The study compared the effect of irradiation by a 650-nm Ga-Al-As laser with LLLT doses of 2.6 Joules/cm(2) to celecoxib, dexamethasone, and control groups for hemorrhagic index (HI) and myeloperoxide activity (MPO) at 24 h after injury. RESULTS: The HI for the control group was 4.0 (95% CI, 3.7-4.3). Celecoxib, LLLT, and dexamethasone all induced significantly (p < 0.01) lower HI than control animals at 2.5 (95% CI, 1.9-3.1), 1.8 (95% CI, 1.2-2.4), and 1.5 (95% CI, 0.9-2.1), respectively, for all comparisons to control. Dexamethasone, but not celecoxib, induced a slightly, but significantly lower HI than LLLT (p = 0.04). MPO activity was significantly decreased in groups receiving celecoxib at 0.87 (95% CI, 0.63-1.11), dexamethasone at 0.50 (95% CI, 0.24-0.76), and LLLT at 0.7 (95% CI, 0.44-0.96) when compared to the control group, at 1.6 (95% CI, 1.34-1.96; p < 0.01), but there were no significant differences between any of the active treatments. CONCLUSION: LLLT at a dose of 2.6 Joules/cm(2) induces a reduction of HI levels and MPO activity in hemorrhagic injury that is not significantly different from celecoxib. Dexamethasone is slightly more effective than LLLT in reducing HI, but not MPO activity.

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A 32 year old man was admitted for dyspnea, hemoptysis, macroscopic hematuria, hypertension (140/100), peripheral edema and hemodynamic decompensation. Lung Xrays revealed pulmonary edema and a cavity in the left apex. Laboratory determinations revealed an altered renal function with increased creatinine and urea levels and nephrotic syndrome. There was leucocyturia, hematuria and cylindruria. The sputum showed a large number of acid-fast bacilli. The patient began anti-tuberculosis treatment with three drugs (isoniacid, rifampicin, pirazinamide). On ultrasonography, both kidneys revealed ecogenic lesions with size, shape and cortico-medular relationship preserved. The patient persisted with altered renal function, steady levels of urea nitrogen, creatinine and potassium, preserved diuresis and hypertension. Bidimensional echocardiogram: LVDD 55 mm, hypoquinetic septum, pericardic effusion, thickened pericardium, pleural effusion, shortening fraction decreased. He received treatment for this congestive cardiac failure and hypertension with enalapril, nifedipine and fursemide. A percutaneous renal biopsy was performed with anatomopathologic diagnosis of diffuse encocapillar proliferative glomerulonephritis with crescents (15%) and total glomerular sclerosis (33%). Immunofluorescence: positive, immune-complexes with IgM and C3. The patient gradually recovered his normal renal function, improved his pleural effusions and normalized his cardiac function. He was discharged in good clinical condition on the 69th day of anti-tuberculosis treatment. An association between pulmonary tuberculosis and glomerulonephritis is discussed. It is proposed that renal lesions might be the consequence of the tuberculosis due to the sedimentation of circulating immune-complexes.

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Se presenta el caso de un varón de 32 años que ingresó por dispnea de esfuerzo, hemoptisis, hematuria macroscópica, hipertensión, edemas perifáricos y descompensación hemodinámica con radiología compatible con edema de pulmón y cavidad en vértice izquierdo. Los exámines de laboratorio mostraron función renal alterada con cifras elevadas de urea y creatinina y síndrome nefrótico. Se encontró leucocituria, hematuria y cilindruria intensas. Se hizo diagnóstico de tuberculosis pulmonar por baciloscopía positiva comenzando tratamiento tuberculostático. El paciente persistió con su función renal gravada con cifras estables de uremia, creatininemia y potasemia con ritmo diurético conservado e hipertenso. Se efectuó punción-biopsia renal con diagnóstico anatomopatológico de glomerulonefritis proliferativa difusa endocapilar con formación de semilunas (15 por ciento) y esclerosis glomerular total (33 por ciento). Por inmunofluorescencia se detectaron depósitos difusos de inmunocomplejos granulares localizados en mesangio, con positividad IgM ++ C3 +. El paciente se recuperó gradualmente hacia una función renal normal, disminuyó sus derrames pleurales y normalizó su función cardíaca con el tratamiento tuberculostático. Se comenta la asociación entre glomerulonefritis y tuberculosis pulmonar a la luz de la bibliografía disponible y se sugiere una relación causal entre ambas entidades

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Se presenta el caso de un varón de 32 años que ingresó por dispnea de esfuerzo, hemoptisis, hematuria macroscópica, hipertensión, edemas perifáricos y descompensación hemodinámica con radiología compatible con edema de pulmón y cavidad en vértice izquierdo. Los exámines de laboratorio mostraron función renal alterada con cifras elevadas de urea y creatinina y síndrome nefrótico. Se encontró leucocituria, hematuria y cilindruria intensas. Se hizo diagnóstico de tuberculosis pulmonar por baciloscopía positiva comenzando tratamiento tuberculostático. El paciente persistió con su función renal gravada con cifras estables de uremia, creatininemia y potasemia con ritmo diurético conservado e hipertenso. Se efectuó punción-biopsia renal con diagnóstico anatomopatológico de glomerulonefritis proliferativa difusa endocapilar con formación de semilunas (15 por ciento) y esclerosis glomerular total (33 por ciento). Por inmunofluorescencia se detectaron depósitos difusos de inmunocomplejos granulares localizados en mesangio, con positividad IgM ++ C3 +. El paciente se recuperó gradualmente hacia una función renal normal, disminuyó sus derrames pleurales y normalizó su función cardíaca con el tratamiento tuberculostático. Se comenta la asociación entre glomerulonefritis y tuberculosis pulmonar a la luz de la bibliografía disponible y se sugiere una relación causal entre ambas entidades (AU)

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With the idea in mind to review the etiologic characteristics and evolution of nonbacterial acute tubulointerstitial nephritis, 29 cases seen at the Hospital Infantil de México between 1972 and 1978 were studied. The ages of patients fluctuated from 3 months to 14 years; 18 of them were males. The disease was associated with the administration of nephrotoxic agents, fundamentally antibiotics, being in order of frequency; gentamicin, kanamycin, ampicillin and streptomycin. The main initial manifestations were hematuria and oliguria. At the onset of the disease, acute renal failure was found in 5 of the patients. Two patients developed chronic renal failure, which in one of them was caused by diphenylhydantoin and was reversible on discontinuance of the drug. There were 3 deaths which in 2 cases followed infectious complication and in 1, renal failure. Considerations are made on the pathogenesis of the disease which is predominantly immunologic of following direct toxic action.

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Decreased synthesis (hypomorphism) of the fast variant of the third component of complement was detected in three generations of a family in which the propositus has an immune complex-type glomerulonephritis, arthritis, and a false positive test for syphilis. An affected sibling has bursitis, hematuria, and proteinuria. Decreased serum C3 protein was detected in three of four and decreased C3H50 in four of four family members with this hypomorphic variant (C3f). This is the first association between C3f and immune complex-type disease.

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