A link between circulating immune complexes and acute kidney injury in human visceral leishmaniasis.

Visceral leishmaniasis (VL) is an infectious disease caused by Leishmania infantum. Clinically, VL evolves with systemic impairment, immunosuppression and hyperactivation with hypergammaglobulinemia. Although renal involvement has been recognized, a dearth of understanding about the underlying mechanisms driving acute kidney injury (AKI) in VL remains. We aimed to evaluate the involvement of immunoglobulins (Igs) and immune complexes (CIC) in the occurrence of AKI in VL patients. Fourteen VL patients were evaluated between early treatment and 12 months post-treatment (mpt). Anti-Leishmania Igs, CIC, cystatin C, C3a and C5a were assessed and correlated with AKI markers. Interestingly, high levels of CIC were observed in VL patients up to 6 mpt. Concomitantly, twelve patients met the criteria for AKI, while high levels of cystatin C were observed up to 6 mpt. Plasmatic cystatin C was positively correlated with CIC and Igs. Moreover, C5a was correlated with cystatin C, CIC and Igs. We did not identify any correlation between amphotericin B use and kidney function markers in VL patients, although this association needs to be further explored in subsequent studies. Our data reinforce the presence of an important renal function impairment during VL, suggesting the involvement of Igs, CIC, and C5a in this clinical condition.

Immunopathology of Acute Kidney Injury in Severe Malaria.

Acute kidney injury (AKI) is a common feature of severe malaria, and an independent risk factor for death. Previous research has suggested that an overactivation of the host inflammatory response is at least partly involved in mediating the kidney damage observed in P. falciparum patients with AKI, however the exact pathophysiology of AKI in severe malaria remains unknown. The purpose of this mini-review is to describe how different aspects of malaria pathology, including parasite sequestration, microvascular obstruction and extensive intravascular hemolysis, may interact with each other and contribute to the development of AKI in severe malaria, by amplifying the damaging effects of the host inflammatory response. Here, we highlight the importance of considering how the systemic effects and multi-organ involvement of malaria are intertwined with the localized effects on the kidney.

Complications of Sub-microscopic Plasmodium vivax Malaria among Orang Asli in Pos Lenjang, Kuala Lipis.

In recent years, increasing cases of Plasmodium vivax complications had been reported all over the world. This former benign Plasmodium species is now recognized to be one of the human malaria parasites that can produce severe disease. In this article, we report two cases of sub-microscopic P. vivax malaria confirmed by PCR. Both patients were asymptomatic before treatment. They showed unusual presentations few days after initiation of antimalarial treatment. Both patients had subsequently completed antimalarial treatment and recovered completely.

Acute kidney injury associated with intestinal infection by Cyclospora cayetanensis in a kidney transplant patient. A case report.

This study shows a clinical case report of a kidney transplant patient who traveled from Mexico to The Netherlands and ate green vegetables in an international food restaurant. After 5 days, he started having diarrhea, nausea, colic, and a physical feeling of malaise. The patient only received symptomatic treatment after showing the characteristic symptoms of traveler's diarrhea. When he returned to Mexico, the clinical picture worsened, and he was hospitalized. Clinical analyses indicated dehydration and acute kidney injury stage II. Coproparasitoscopic study showed the presence of Cyclospora cayetanensis. Parenteral solutions, gastric mucosal protector, ciprofloxacin, and a soft diet were administrated as treatment. The patient was discharged 72 h later with an improvement of the kidney function.

Metabolic profiling during malaria reveals the role of the aryl hydrocarbon receptor in regulating kidney injury.

Systemic metabolic reprogramming induced by infection exerts profound, pathogen-specific effects on infection outcome. Here, we detail the host immune and metabolic response during sickness and recovery in a mouse model of malaria. We describe extensive alterations in metabolism during acute infection, and identify increases in host-derived metabolites that signal through the aryl hydrocarbon receptor (AHR), a transcription factor with immunomodulatory functions. We find that Ahr-/- mice are more susceptible to malaria and develop high plasma heme and acute kidney injury. This phenotype is dependent on AHR in Tek-expressing radioresistant cells. Our findings identify a role for AHR in limiting tissue damage during malaria. Furthermore, this work demonstrates the critical role of host metabolism in surviving infection.

Fracaso renal agudo anúrico persistente en paciente infectado con Plasmodium malariae: la importancia de la biopsia renal / Persistent acute renal failure in a patient infected with Plasmodium malariae: The importance of renal biopsy

No disponible

Malaria, Collapsing Glomerulopathy, and Focal and Segmental Glomerulosclerosis.

BACKGROUND AND OBJECTIVES: Malaria, a potentially life-threatening disease, is the most prevalent endemic infectious disease worldwide. In the modern era, the spectrum of glomerular involvement observed in patients after malarial infections remains poorly described. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: We therefore performed a retrospective multicenter study to assess the clinical, biologic, pathologic, and therapeutic characteristics of patients with glomerular disease demonstrated by kidney biopsy in France within 3 months of an acute malaria episode. RESULTS: We identified 23 patients (12 men), all but 1 of African ancestry and including 10 patients with concomitant HIV infection. All of the imported cases were in French citizens living in France who had recently traveled back to France from an endemic area and developed malaria after their return to France. Eleven patients had to be admitted to an intensive care unit at presentation. Plasmodium falciparum was detected in 22 patients, and Plasmodium malariae was detected in 1 patient. Kidney biopsy was performed after the successful treatment of malaria, a mean of 24 days after initial presentation. At this time, all patients displayed AKI, requiring KRT in 12 patients. Nephrotic syndrome was diagnosed in 17 patients. Pathologic findings included FSGS in 21 patients and minimal change nephrotic syndrome in 2 patients. Among patients with FSGS, 18 had collapsing glomerulopathy (including 9 patients with HIV-associated nephropathy). In four patients, immunohistochemistry with an antibody targeting P. falciparum histidine-rich protein-2 demonstrated the presence of the malaria antigen in tubular cells but not in podocytes or parietal epithelial cells. An analysis of the apoL1 risk genotype showed that high-risk variants were present in all seven patients tested. After a mean follow-up of 23 months, eight patients required KRT (kidney transplantation in two patients), and mean eGFR for the other patients was 51 ml/min per 1.73 m2. CONCLUSIONS: In patients of African ancestry, imported Plasmodium infection may be a new causal factor for secondary FSGS, particularly for collapsing glomerulopathy variants in an APOL1 high-risk variant background.

Acute kidney injury in pediatric patients with malaria: A prospective cross-sectional study in the shai-osudoku district of Ghana.

Acute kidney injury (AKI) is a highly fatal complication of malaria. We used the Kidney Disease Improving Global Outcomes (KDIGO) and Pediatric Risk, Injury, Failure, Loss, End-Stage Kidney Disease (pRIFLE) guidelines to assess AKI among children. One hundred children with Plasmodium falciparum malaria were recruited from the St. Andrew's Catholic Hospital. Admission and 48-h serum creatinine were estimated. Weight and height of the participants were measured, and AKI status determined with the KDIGO and pRIFLE guidelines. A questionnaire was used to collect the socio-demographic and clinical data of participants. Two percent and 5% of the participants had AKI according to the KDIGO and pRIFLE criteria, respectively. Per the KDIGO guidelines, 1% of the participants had Stage 2 and 1% also had Stage 3 AKI. Four percent had Stage 1 (risk) and 1% had Stage 2 (injury) AKI per the pRIFLE criteria. Participants with AKI were dehydrated, and neither had sepsis or on antibiotics when the KDIGO guideline was used. Participants who had AKI were dehydrated, with 80% having sepsis and 40% on antibiotics when the pRIFLE criteria were used. There was no association between the KDIGO and pRIFLE criteria with respect to AKI status of participants (k = -0.029, P = 0.743). Two percent and 5% of the study participants had AKI when the KDIGO and pRIFLE guidelines were used respectively. One percent of the participants had Stage 2 and 1% also had Stage 3 AKI per KDIGO; 4% had Stage 1 (risk) and 1% had Stage 2 (injury) AKI per the pRIFLE.

Evaluation of acute kidney injury in dogs with complicated or uncomplicated Babesia rossi infection.

Dogs with babesiosis can present with multiple complications, including acute kidney injury (AKI). The objective of this study was to characterize AKI in dogs with babesiosis caused by Babesia rossi at presentation and after treatment. Thirty-five client-owned dogs with B. rossi infection and 10 control dogs were included in this prospective observational study. Blood and urine were collected in Babesia-infected dogs at presentation (T0, n = 35), after 24 h (T24h, n = 11), and after 1 month (T1m, n = 9). The following urinary kidney injury biomarkers were assessed: urinary protein to creatinine ratio (UPC), urinary glomerular injury biomarkers (immunoglobulin G (uIgG) and C-reactive protein (uCRP)), and urinary tubular injury biomarkers (retinol-binding protein (uRBP) and neutrophil gelatinase-associated lipocalin (uNGAL)). Serum functional renal biomarkers were creatinine (sCr) and symmetric dimethylarginine (sSDMA). Post-mortem kidney biopsies were analyzed by light and transmission electron microscopy. At T0, all kidney injury biomarkers were significantly higher in Babesia-infected dogs compared to healthy controls (P < 0.001), while functional renal biomarkers were not significantly different (P > 0.05). At T24h, all urinary tubular injury biomarkers and UPC decreased significantly (P < 0.01), while glomerular injury biomarkers did not (P = 0.084). At T1m, all urinary kidney injury biomarkers decreased to values not significantly different from healthy controls (P > 0.5). Significant changes in functional renal biomarkers were not seen after treatment (P > 0.05). Dogs with complicated babesiosis had significantly higher glomerular injury biomarkers, UPC, and sSDMA compared to uncomplicated cases (P < 0.05), while all tubular injury biomarkers and sCr were not significantly different (P > 0.1). Dogs with babesiosis caused by B. rossi showed transient kidney injury, which was detected by all kidney injury biomarkers, but remained undetected by functional biomarkers. All infected dogs, irrespective of disease severity, suffered comparable kidney injury based on tubular injury biomarker concentrations, while loss of function was seen more often in dogs with complicated babesiosis based on sSDMA results.

Renal detection of Plasmodium falciparum, Plasmodium vivax and Plasmodium knowlesi in malaria associated acute kidney injury: a retrospective case-control study.

OBJECTIVE: Acute kidney injury (AKI) is a frequent presentation in malaria infections. Several cases of AKI that are accompanied by clinical symptoms of malaria infection, such as fever, nausea, respiratory distress, and anemia remain undiagnosed due to challenges in accurate diagnosis using peripheral blood microscopy and rapid diagnostic tests that are currently used in clinical settings. This is particularly true for P. vivax and P. knowlesi infections. As a result, these patients are not able to receive anti-malarial therapy in a timely manner. The objective of the present study was to investigate if patients presenting with AKI harbored any of the five human Plasmodium species (P. falciparum, P. vivax, P. knowlesi, P. malariae, and P. ovale) within their renal tissues. RESULTS: We found that renal biopsies from malaria associated AKI patients harbor the human malaria parasites P. falciparum, P. vivax and P. knowlesi as mono- and mixed species infections. Presence of microvascular injury in a majority of the malaria associated AKI cases suggested vascular involvement of P. vivax and P. knowlesi. This research note also highlights P. knowlesi as an emerging pathogen in the Indian subcontinent.

Acute Kidney Injury in Children with Severe Malaria Is Common and Associated with Adverse Hospital Outcomes.

BACKGROUND: The prevalence of acute kidney injury (AKI) in children with severe malaria in sub-Saharan African may have been underestimated. The study aimed to determine the prevalence of AKI in children with severe malaria and its association with adverse hospital outcomes. METHODS: At presentation, we measured complete blood count, serum bilirubin, and serum electrolytes, urea and creatinine in children with severe malaria. At 24 h after hospitalization, we repeated serum creatinine measurement. Urine passed in the first 24 h of hospitalization was also measured. We defined AKI and its severity using the Kidney Disease: Improving Global Outcome AKI guidelines. RESULTS: The study involved 244 children (53.3% males) with a median age of 3.5 (1.9-7.0) years. One hundred and forty-four (59%) children had AKI, and it reached maximum Stages 1, 2 and 3 in 56 (23%), 45 (18.4%) and 43 (17.6%) children, respectively. The majority (86.1%) with AKI had only elevated serum creatinine. Mortality increased with increasing severity of AKI on univariate analysis but weakened on multiple logistic regression. Mortality was also higher in those with both oliguria and elevated serum creatinine than in those with elevated serum creatinine only (50% vs. 4.8%, p < 0.001). Furthermore, children with AKI spent three days more in hospital than those without AKI (p < 0.001). CONCLUSIONS: Acute kidney injury complicates severe malaria in 6 out of every 10 children and is commonly identified using elevated serum creatinine. It is also associated with adverse hospital outcome.

Acute Kidney Injury Induced by Pneumoperitoneum Pressure Via a Mitochondrial Injury-dependent Mechanism in a Rabbit Model of Different Degrees of Hydronephrosis.

OBJECTIVE: To clarify the effect of mitochondrial injury during laparoscopic surgery of the kidney in different degrees of hydronephrosis in rabbit model. METHODS: A total of 90 rabbits were randomly allocated into 3 groups (groups PN, PM, and PS, ie, rabbits without, with mild and with severe hydronephrosis, respectively). The rabbits in the PM group (n = 30) and PS group (n = 30) underwent surgical procedures that induced mild and severe left hydronephrosis, respectively. The rabbits in all the groups were then allocated into 5 subgroups and were subjected to intra-abdominal pressures of 0, 6, 9, 12, and 15 mmHg. Changes in the mitochondrial membrane potential and mitochondrial electron microstructure were observed. The apoptosis proteins cytochrome C, apoptosis-inducing factor, caspase-3, and caspase-9 were measured by western blot analysis. RESULTS: As the degrees of hydronephrosis increased, histopathological changes such as the decrease in mitochondrial membrane potential and mitochondrial vacuolization along with increased expression of apoptosis proteins, cytochrome C, apoptosis-inducing factor, caspase-3 gained statistically significance at lower intra-abdominal pressures (In PN and PM groups at 15 mmHg, and in PS group at 9 mmHg; for all P <.01). CONCLUSION: Mitochondrial injury plays an important role during acute kidney injury induced by pneumoperitoneal pressure in different degrees of hydronephrosis in the rabbit model.

Diagnostic performance of salivary urea nitrogen dipstick to detect and monitor acute kidney disease in patients with malaria.

BACKGROUND: Acute kidney injury (AKI) is a common complication of malaria. In low resource settings, a lack of diagnostic tools and delayed treatment of malaria associated AKI lead to significant morbidity and mortality. The aim of this study was to assess the diagnostic performance of salivary urea nitrogen (SUN) dipstick to detect and monitor kidney disease [KD = AKI or acute kidney disease (AKD) without AKI] in malaria patients in Angola. METHODS: Patients 11-50 years old admitted with malaria at the Josina Machel (Maria-Pia) Hospital, Luanda, Angola, between 2nd March and 10th May 2016 were enrolled in this study. All participants had serum creatinine (sCr), blood urea nitrogen (BUN) and SUN dipstick tested at the time of recruitment and daily for up to 4 days. AKD without AKI refers to acute renal impairment which do not fulfilled the main criteria for AKI (increases in the baseline serum creatinine and/or decreases in urine output) according defined by the kidney disease improving global outcomes (KDIGO) guideline. RESULTS: Eight-six patients were admitted with malaria diagnosis (mean age 21.5 ± 9.4 years, 71% male) and 27 (32%) were diagnosed with KD. The mean (± SD) sCr and BUN of the KD group at admission (day 0) were 5.38 (± 5.42) and 99.4 (± 61.9) mg/dL, respectively. Three (3.5%) patients underwent haemodialysis and eight (9.3%) died within the first 4 days of hospital admission [5 (62.5%) with KD; 3 (37.5%) without kidney disease; p = 0.047]. The SUN threshold for KD diagnosis was tested pad #5 (SUN > 54 mg/dL). At this threshold, the SUN dipstick had a sensitivity of 67% and specificity of 98% to diagnose KD. The area under the receiver operating characteristics curve (ROC) for KD diagnosis on admission was 0.88 (95% CI 0.79-0.96). The SUN dipstick was most accurate at higher levels of BUN. CONCLUSION: The SUN dipstick had reasonable sensitivity and excellent specificity when used to diagnose KD in a cohort of patients with malaria in a resource-limited setting. Given the severity of presenting illness and kidney injury, the SUN dipstick diagnostic threshold was high (test pad #5). SUN may be used to detect AKI in patients with malaria in low resources settings, thus facilitating earlier access to adequate treatment, which may improve survival.

Renal dysfunction in Leishmaniasis and Chagas disease coinfection: a case report.

Visceral leishmaniasis (VL) is an endemic parasitic disease frequently found in Northeast Brazil and may cause acute kidney injury (AKI) and glomerulonephritis. After appropriate treatment, renal function recovery may occur. We describe the rare case of a patient with VL, who developed severe AKI requiring dialysis and was subsequently diagnosed with Chagas disease coinfection. After specific treatment for VL, there was partial recovery of the renal function, followed by the onset of Chagas disease cardiomyopathy.

Visceral leishmaniasis-associated nephropathy in hospitalised Brazilian patients: new insights based on kidney injury biomarkers.

OBJECTIVE: To evaluate the usefulness of early acute kidney injury (AKI) biomarkers in clinical management of visceral leishmaniasis. METHODS: Prospective study with 50 hospitalised VL patients. AKI biomarkers, that is, serum and urinary neutrophil gelatinase-associated lipocalin (sNGAL, uNGAL, respectively), urinary kidney injury molecule-1 (uKIM-1) and urinary monocyte chemotactic protein-1 (uMCP-1), were quantified by immunoassay (ELISA). Also, interferon-gamma (INF-y) and C-reactive protein (CRP) were evaluated as inflammatory biomarkers possibly related to VL severity. RESULTS: VL patients had hyponatremia, hypoalbuminemia, hypergammaglobulinemia, haematologic and hepatic disorders. AKI was found in 46%, and one death (2%) occurred. The AKI group had significant longer hospital stay, lower levels of IFN-y and higher levels of CRP, more clinical renal abnormalities and higher levels of sNGAL, uNGAL, uKIM-1 and uMCP-1. Overall, sNGAL, uKIM-1 and uMCP-1 showed correlations with important clinical renal abnormalities, such as proteinuria, albuminuria, serum creatinine and glomerular filtration rate using adjusted correlations with CRP and IFN-y. Only sNGAL showed an early association with AKI development (OR = 2.78, 95% CI = 1.429-5.428, per each increase of 50 ng/ml), even after adjusting for clinical signals of VL severity and for immune biomarkers. Moreover, sNGAL showed a better performance in predicting AKI development (AUC-ROC = 0.81, 95% CI = 0.69-0.93; cut-off = 154 ng/ml, sensitivity = 82.6%, specificity = 74.1%, P < 0.001). CONCLUSIONS: Visceral leishmaniasis-associated nephropathy showed important proximal tubular injury and glomerular inflammation. Serum NGAL showed an early association with VL-associated nephropathy and may be used to improve clinical management strategies and decrease morbimortality in VL patients.

Age-Related Clinical Spectrum of Plasmodium knowlesi Malaria and Predictors of Severity.

Background: Plasmodium knowlesi is increasingly reported in Southeast Asia, but prospective studies of its clinical spectrum in children and comparison with autochthonous human-only Plasmodium species are lacking. Methods: Over 3.5 years, we prospectively assessed patients of any age with molecularly-confirmed Plasmodium monoinfection presenting to 3 district hospitals in Sabah, Malaysia. Results: Of 481 knowlesi, 172 vivax, and 96 falciparum malaria cases enrolled, 44 (9%), 71 (41%), and 31 (32%) children aged ≤12 years. Median parasitemia was lower in knowlesi malaria (2480/µL [interquartile range, 538-8481/µL]) than in falciparum (9600/µL; P < .001) and vivax malaria. In P. knowlesi, World Health Organization-defined anemia was present in 82% (95% confidence interval [CI], 67%-92%) of children vs 36% (95% CI, 31%-41%) of adults. Severe knowlesi malaria occurred in 6.4% (95% CI, 3.9%-8.3%) of adults but not in children; the commenst severity criterion was acute kideny injury. No patient had coma. Age, parasitemia, schizont proportion, abdominal pain, and dyspnea were independently associated with severe knowlesi malaria, with parasitemia >15000/µL the best predictor (adjusted odds ratio, 16.1; negative predictive value, 98.5%; P < .001). Two knowlesi-related adult deaths occurred (fatality rate: 4.2/1000 adults). Conclusions: Age distribution and parasitemia differed markedly in knowlesi malaria compared to human-only species, with both uncomplicated and severe disease occurring at low parasitemia. Severe knowlesi malaria occurred only in adults; however, anemia was more common in children despite lower parasitemia. Parasitemia independently predicted knowlesi disease severity: Intravenous artesunate is warranted initially for those with parasitemia >15000/µL.

The effect of regularly dosed paracetamol versus no paracetamol on renal function in Plasmodium knowlesi malaria (PACKNOW): study protocol for a randomised controlled trial.

BACKGROUND: Plasmodium knowlesi is the most common cause of human malaria in Malaysia. Acute kidney injury (AKI) is a frequent complication. AKI of any cause can have long-term consequences, including increased risk of chronic kidney disease, adverse cardiovascular events and increased mortality. Additional management strategies are therefore needed to reduce the frequency and severity of AKI in malaria. In falciparum malaria, cell-free haemoglobin (CFHb)-mediated oxidative damage contributes to AKI. The inexpensive and widely available drug paracetamol inhibits CFHb-induced lipid peroxidation via reduction of ferryl haem to the less toxic Fe3+ state, and has been shown to reduce oxidative damage and improve renal function in patients with sepsis complicated by haemolysis as well as in falciparum malaria. This study aims to assess the ability of regularly dosed paracetamol to reduce the incidence and severity of AKI in knowlesi malaria by attenuating haemolysis-induced oxidative damage. METHODS: PACKNOW is a two-arm, open-label randomised controlled trial of adjunctive paracetamol versus no paracetamol in patients aged ≥ 5 years with knowlesi malaria, conducted over a 2-year period at four hospital sites in Sabah, Malaysia. The primary endpoint of change in creatinine from enrolment to 72 h will be evaluated by analysis of covariance (ANCOVA) using enrolment creatinine as a covariate. Secondary endpoints include longitudinal changes in markers of oxidative stress (plasma F2-isoprostanes and isofurans) and markers of endothelial activation/Weibel-Palade body release (angiopoietin-2, von Willebrand Factor, P-selectin, osteoprotegerin) over 72 h, as well as blood and urine biomarkers of AKI. This study will be powered to detect a difference between the two treatment arms in a clinically relevant population including adults and children with knowlesi malaria of any severity. DISCUSSION: Paracetamol is widely available and has an excellent safety profile; if a renoprotective effect is demonstrated, this trial will support the administration of regularly dosed paracetamol to all patients with knowlesi malaria. The secondary outcomes in this study will provide further insights into the pathophysiology of haemolysis-induced oxidative damage and acute kidney injury in knowlesi malaria and other haemolytic diseases. TRIAL REGISTRATION: Clinicaltrials.gov, NCT03056391 . Registered on 12 October 2016.

Renal dialysis and long-term treatment of a dog with kidney disease associated with canine leishmaniosis.

BACKGROUND: Renal disease is considered the main cause of natural mortality in dogs with canine leishmaniosis. The pathological mechanisms associated with kidney injury in canine leishmaniosis include immune complex glomerulonephritis, tubulointerstitial nephritis and occasionally renal amyloidosis. Proteinuria is a frequent finding in canine leishmaniosis and its quantification by the urine protein-creatinine ratio (UPC) is an important parameter in the staging of canine lesihmaniosis as presented by the LeishVet group. RESULTS: A 4.5 year-old spayed female Belgian Malinois dog was presented to the Hebrew University Veterinary Teaching hospital with epistaxis and rhinitis and diagnosed also with proteinuria and acute kidney injury (AKI IRIS grade V) associated with canine leishmaniosis that developed to LeishVet stage III with chronic kidney disease (CKD) after stabilization. Clinicopathologic abnormalities included azotemia with a peak creatinine concentration of 7.76 mg/dl (reference interval, 0.3-1.2 ng/dl), hypoalbuminemia (1.76 g/dl, reference interval 3-4.4 g/dl), hyperglobulinemia (4.54 g/dl, reference interval 1.8-3.9 g/dl) and proteinuria (urine protein/creatinine ratio 15.6, normal < 0.2). Serology by the enzyme-linked immunosorbent assay (ELISA) for Leishmania infantum was positive with high antibody levels. The dog was hospitalized and treated with intermittent hemodialysis, feeding through an esophageal feeding tube, medical treatment for protein losing nephropathy and antileishmanial treatment with allopurinol. Kidney function gradually improved and the dog's creatinine levels and proteinuria decreased until complete normalization two years after the acute insult. However, rhinitis and sneezing persisted and although the anti-leishmanial antibodies decreased over time, the dog remains constantly seropositive. CONCLUSIONS: To our knowledge, this is the first report of hemodialysis management of AKI associated with canine leishmaniosis. Hemodialysis was imperative in stabilizing the dog's renal disease and controlling its azotemia. It demostrates that hemodialysis can be beneficial in the management of acute deterioration of kidney disease in canine leishmaniosis.