Biomarkers and renal arterial resistive index in dogs naturally infected with Leishmania infantum.

Canine visceral leishmaniasis frequently causes glomerulonephritis and tubulointerstitial nephritis, nephropathies for which diagnosis has been limited by the low sensitivity of traditional tests. The aim of this study was to evaluate serum cystatin C and urinary gamma-glutamyltransferase (uGGT) levels and the urinary GGT/urinary creatinine ratio (uGGT/uCR) and to measure the renal arterial resistive index (RARI) in dogs with leishmaniasis with varying degrees of renal injury based on the urine protein: creatinine ratio (UP/C) and serum creatinine (SCr) level. We tested 59 untreated adult dogs of both sexes and undefined breeds naturally infected with Leishmania infantum. The dogs were grouped into four groups based on UP/C and SCr level: group 1 (n = 15), dogs with SCr levels < 1.4 mg/dL and UP/C < 0.5; group 2 (n = 13), dogs with SCr levels < 1.4 mg/dL and UP/C of 0.5-1.0; group 3 (n = 16), dogs with SCr levels < 1.4 and UP/C > 1.0; and group 4 (n = 15), dogs with SCr levels > 1.4. A fifth group of healthy dogs (n = 10) was the control. uGGT concentrations and uGGT/uCR were higher in dogs with proteinuria and SCr < 1.4 mg/dL, whereas the serum cystatin C concentrations and RARI were higher only in dogs with SCr levels > 1.4. In conclusion, uGGT and uGGT/uCR may be useful tools for early detection and assessment of renal lesions associated with leishmaniasis; however, cystatin C is useful for monitoring the progression of kidney disease when measured sequentially.

Hydatid disease and tubulointerstitial nephritis.

Hydatid disease of the kidney is rare, particularly in the isolated form, and tubulointerstitial nephritis is an extremely uncommon manifestation of renal hydatidosis. Here is the report of a patient with isolated renal hydatid disease who presented with acute renal failure secondary to tubulointerstitial nephritis. The patient responded to the combination of albendazole, corticosteroids and total nephrectomy.

Visceral leishmaniasis in a kidney transplant recipient: parasitic interstitial nephritis, a cause of renal dysfunction.

Visceral leishmaniasis (VL) due to Leishmania infantum is an endemic parasitic infection in the Mediterranean area. It most commonly affects immunosuppressed individuals, especially HIV patients and less frequently organ transplant recipients. Renal involvement seems to be frequent and is mostly associated with tubulointerstitial nephritis, as described in autopsy reports. In the 61 cases of renal transplant recipients with VL reported in the literature, renal dysfunction was noted at clinical presentation and was more frequently observed as a complication of antiparasitic therapy. However, no pathological analysis of the allograft lesions was reported. We present the case of a Swiss renal transplant recipient who developed VL after vacations in Spain and Tunisia, complicated by acute parasitic nephritis in the renal allograft 3 months after a well-conducted treatment of liposomal amphotericin B.

Collapsing Focal Segmental Glomerulosclerosis with Acute Interstitial Nephritis Associated with Plasmodium Falciparum: A Case Report and Review of the Literature.

BACKGROUND Malaria adversely affects the kidney in a variety of ways. The most common kidney injury is acute tubular necrosis, although various glomerular lesions are also described. Of these, collapsing focal segmental glomerulosclerosis (cFSGS) is the most rarely seen. Thus, the natural history of this lesion and response to treatment are not clear. Herein, we present a case of cFSGS complicated by acute interstitial nephritis caused by Plasmodium falciparum (P. falciparum) unresponsive to prednisone. CASE REPORT A 64-year-old Nigerian man with chronic kidney disease due to hypertensive nephropathy was admitted to the hospital, diagnosed with active P. falciparum malaria infection after returning from Nigeria. He developed acute kidney injury and nephrotic range proteinuria. Renal biopsy showed acute interstitial nephritis and cFSGS. Despite corticosteroid therapy, his kidney function worsened, requiring initiation of renal replacement therapy. This is the fifth case report of cFSGS due to malaria P. falciparum but the first to report the presence of acute interstitial nephritis in association with cFSGS due to malaria. CONCLUSIONS cFSGS is rarely seen as a manifestation of P. falciparum infection. When associated with acute interstitial nephritis, the prognosis seems to be worse. It appears that age and co-morbidities are the risk factors for unresponsiveness to corticosteroids, and treatment of the renal disease should focus on rapidly eradicating the parasitemia and providing supportive care. Our case report is the first to describe a combination of cFSGS and interstitial nephritis caused by P. falciparum unresponsive to corticosteroids.

Encephalitozoon infection in a still-born foal.

A stud Clydesdale foal was still-born near full term. Macroscopic examination revealed a normal placenta, pulmonary atelectasis and faint white mottling of the kidneys. Microscopically there was severe lymphoplasmacytic interstitial nephritis. Numerous organisms resembling Encephalitozoon cuniculi were present in the affected kidneys. The organisms occurred in the areas of inflammation as well as in the renal glomeruli and intracellular cysts in the renal tubular epithelial cells and exhibited Gram positive staining. Ultrastructurally the organisms possessed a polar vacuole and a spiral filament typical of Microsporidia. The organisms were not detected in sections of the other organs examined.

Encephalitozoonosis in pet rabbits (Oryctolagus cuniculus): pathohistological findings in animals with latent infection versus clinical manifestation.

Encephalitozoon cuniculi is a common infectious agent of rabbits. The aim of this study was to determine the distribution and extent of histological lesions in the brain and in the kidney of naturally infected pet rabbits with or without clinical encephalitozoonosis. In 71 animals (33 with symptoms) which died or were euthanised, histopathological examination including staining of spores (Ziehl-Neelsen, acid-fast trichrome) was performed and changes were described quantitatively. The cerebrum was the most frequently affected brain region (97.5%), whilst the cerebellum (55%) and the vestibular cores (37.5%) were less commonly concerned. Granulomas were found in 77.5% of animals with encephalitis and in 12.5% of rabbits with interstitial nephritis. Although cerebral granulomas were found irrespective of the grade of histological changes, they were significantly correlated with changes at higher grades. There was no correlation between the severity of encephalitis and neurological symptoms. Since severe lesions were also found in clinically inconspicuous animals, histological findings of inflammatory lesions are not indicative of overt encephalitozoonosis as the causative agent for neurological signs. Other diseases causing neurological symptoms, such as suppurative encephalitis, otitis media as well as malignant lymphoma were also detected in the rabbit population that was examined in the present study.

[Renal glomerular lesions and Plasmodium falciparum infection]. / Atteinte glomérulaire rénale et infection à Plasmodium falciparum.

Following the study done in 1990 concerning the existence of glomerular lesions in falciparum malaria, this study, pursued on large scale, included 110 persons (30 healthy persons, 11 other than falciparum malaria, and 69 cases of falciparum malaria). 30.4% among these 69 cases of falciparum malaria presented glomerular affect signs. A complete clinical and biological recovery was obtained with quinine injection.

Dysregulation of cytokine expression in tubulointerstitial nephritis associated with murine malaria.

We examined the circulating levels of the proinflammatory cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 alpha, IL-6, granulocyte macrophage-colony stimulating factor (GM-CSF), and the anti-inflammatory cytokine IL-10, and their expression in kidneys acutely infected with murine malaria parasite P. berghei ANKA in C57BL/6J mice. Groups of six mice sacrificed on days 5, 10, 15, and 20, and normal controls were used for cytokine analysis. High concentrations of TNF-alpha and IL-10 were detected in plasma as shown by ELISA, and elevated levels of mRNA specific for TNF-alpha and IL-10 in infected kidneys were demonstrated by reverse transcription-polymerase chain reaction (RT-PCR) analysis. Kidney sections stained with antibodies against TNF-alpha, IL-1 alpha, IL-6, GM-CSF and IL-10 for immunohistochemistry showed markedly enhanced staining for TNF-alpha, and progressively increased staining for IL-1 alpha and IL-6 both in the tubules and the walls of arteries during the course of infection. The endothelia of blood vessels and inflammatory cells located around small arteries showed positive staining for GM-CSF from day 10 onwards. Unlike the staining for proinflammatory cytokines, the anti-inflammatory cytokine IL-10 showed strongly positive staining in normal tubules and walls of arteries, especially in the brush border of proximal tubules, but the staining intensity decreased dramatically after day 15 post-infection. A strongly positive correlation was found between the antibody staining for TNF-alpha/IL-1 alpha in tubules, and the severity of proteinuria. In contrast, there was an inverse correlation between the staining for IL-10 with TNF-alpha/IL-1 alpha, and the degree of proteinuria. Plenty of pigmented macrophages showed positive staining both for proinflammatory and anti-inflammatory cytokines in the tubulointerstitium. Our findings imply that the up-regulation of proinflammatory cytokines and the dysregulation of anti-inflammatory cytokines are involved in the pathogenesis of tubulointerstitial nephritis associated with malaria.