Acute kidney injury as initial presentation of visceral leishmaniasis in a young patient- A case report.

Introduction: Visceral leishmaniasis is endemic in Somalia and in East Africa at large. Clinically, patients present with recurrent fever, weight loss, hepatosplenomegaly and pancytopenia. Sometimes, patients in low resource countries with no properly functioning primary healthcare facilities may present with complications. Case presentation: Here, we report a case of 19 years old male patient who presented with impaired renal function. After diagnosing with VL and starting Sodium Stibogluconate, patient developed acute pancreatitis, that compelled us to shift to liposomal amphotericin B, which he responded well and finally was discharged within a good condition. Clinical discussion: Early diagnosis and proper treatment is necessary to restore the renal function.
Conclusion: This case report elaborates some of the clinical presentations of VL, complications of treatment and encouraging physicians in endemic areas to keep VL into their list of differential diagnosis in patients with fever and hepatosplenomegaly.

Introductions

The protozoan Leishmania donovani causes chronic infectious disease called Visceral leishmaniasis (VL), also known as Kala-azar. It's more prevalent in tropical and subtropical areas. leishmaniasis, mucocutaneous leishmaniasis, VL, and post-kala-azar dermal leishmaniasis are the four main clinical syndromes caused by over 20 different leishmanial species. [1]. The most common form of leishmaniasis is cutaneous leishmaniasis.VL causes about 20,000 to 30,000 deaths each year worldwide and its second-largest parasitic killer in the world after malaria [2].After the Indian subcontinent, East Africa has the highest burden [3]. This fatal parasite disease has mostly been reported in regions of southern Somalia, although data from Somalia is limited, and the exact scale of the VL burden is unknown.

In the East Mediterranean Region (EMR), leishmaniasis is a major public health concern. In 2008, 12 countries in the EMR reported 100,000 new cases of cutaneous leishmaniasis to WHO (EMR). In terms of Anthroponotic visceral leishmaniasis (AVL), Sudan and Somalia documented 4108 and 583 cases, respectively [4].

Clinical presentation dependents on both the infecting species of Leishmania and the host's immune response. Persistent fever, splenomegaly and pancytopenia are the chief characteristicsof visceral leishmaniasis [5].

The microscopic detection of the parasite in patient's tissue remains the gold standard for diagnosis. Despite splenic rupture been the most sensitive technique, lymph-node and bone aspirate can be used with lower sensitivity [6].

Renal involvement of VL is a well-known and can present as acute or chronic renal insufficiency. Here, we present the first documented and successfully managed case of acute kidney injury due to VL.

Case report

A 19-year-old male patient from El-Barde District, southwestern Bakool region of Somalia, presented to our hospital with a three-month history of intermittent fever, fatigue, generalized weakness and loss of appetite for one month. He took local symptomatic treatment and anti-malaria medications, but did not get any relief. The general physical examination showed a febrile patient, pulse rate of 106 beats/min, respiratory rate of 16 breaths/min and blood pressure of 125/70 mm Hg and appeared pale. Abdominal examination revealed splenomegaly and hepatomegaly. The remaining part of the examination was normal. Initial blood tests revealed WBC 1400/mm3 (normal 4000–10,000/mm3), hemoglobin 5.1 g/dL (normal 13–17 g/dL), hematocrit 16.2% (normal 42–52%), platelet 11 × 1000/mm3 (normal 100–430 × 1000/mm3), serum urea 228 mg/dL (normal 10–45 mg/dL), serum creatinine 4,47 mg/dL (normal 0.6–1.35 mg/dL), aspartate transaminase (AST) 345 U/L (normal 0–35 U/L), alanine transaminase (ALT) 128 U/L (normal 0–45U/L), lactate dehydrogenase (LDH) 2086 U/L (normal 0–248 U/L), blood sugar (random) 87 mg/dL, serum calcium 5,9 mg/dL (normal 8,3–10,6 mg/dL), serum albumin 2,1 g/(normal 3,5 - 5,5 g/dL), serum potassium 6,58 mEq/L (normal 3.5–5.5 mEq/L), CRP 209.28 mg/L (normal 0–10 mg/L). Ultrasonography (USG) of whole abdomen revealed hepatomegaly 20cm, massive splenomegaly 23cm, both kidney sizes were normal with increased parenchymal echogenicity, several reactive lymph nodes and mesenteric thickening were seen in right lower quadrant of abdomen. Computerized tomography (CT) scan of chest revealed cardiomegaly with minimal bilateral pleural effusion and pulmonary edema. Transthoracic echocardiography showed moderate pulmonary hypertension. On the first day of admission, the patient underwent hemodialysis, blood and urine culture was sent, Piperacillin and tazobactam renal dose was started. The viral hepatitis, human immunodeficiency virus, and Brucella serological tests all came back negative. Malaria smear was also negative. Anti-Leishmania antibodies were detected during serological testing with an enzyme-linked immunosorbent assay (ELISA). Patient was started on Sodium stibogluconate 800mg/day. The patient's health worsened, and he developed a recurrent temperature of up to 40 °C. and gum bleeding due to thrombocytopenia, urine and blood culture came out negative, after 4th dose of Sodium stibogluconate, he developed epigastric pain, nausea and vomiting, repeated blood tests revealed amylase 1690 U/L, lipase 3967 U/L, urea 167 mg/dL, creatinine 4.5 mg/dL, LDH 704 U/L. sodium stibogluconate was stopped due acute pancreatitis and patient was kept NPO. After consultation with Infectious diseases, the patient was started on liposomal amphotericin B course (3 mg/kg intravenous on Days 1–5, 14 and 21) with dextrose 5% infusion in 2 hours. After a week, the patient's clinical condition improved, his fever subsided, and his test results improved (Table 1).

Table 1

Summary of patient's laboratory values before and after the treatment.

Before Treatment	After Treatment
WBC 1.40 4–10 × 1000/mm3	WBC 4.07 4–10 × 1000/mm3
HGB 5.1 13–17 g/dL	HGB 9.0 13–17 g/dL
PLT 11,100–430 × 1000/mm3	PLT 278,100–430 × 1000/mm3
MCV 68.0 80–100 fL	MCV 79.3 80–100 fL
Creatinine 4.47 0.6–1.35 mg/dL	Creatinine 0.56 0.6–1.35 mg/dL
Urea 228 10–45 mg/dL	Urea 14 10–45 mg/dL
AST 345 0–35 U/L	AST 45 0–35 U/L
ALT 128 0–45 U/L	ALT 38 0–45 U/L
Albumin 2.1 3.5–5,5 g/dL	Albumin 2.4 3.5–5.5 g/dL
Calcium (Ca) 5.9 8.3–10.6 mg/dL	Calcium (Ca) 8.9 8.3–10.6 mg/dL
Potassium 6.58 3.5–5.5 mEq/L	Potassium 5.73 3.5–5.5 mEq/L
CRP 209.28 0–10 mg/	CRP 11.97 0–10 mg/L

WBC-white blood cells, HGB-hemoglobin, PLT-platelets, MCV-mean corpuscular volume, AST-aspartate transaminase, ALT-alanin transaminase, CRP-C-reactive protein.

Acute kidney injury is diagnosed according to KDIGO Guidelines as any of: Increase in SCr by X0.3 mg/dL (X26.5 lmol/l) within 48 hours; or increase in SCr to X1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or Urine volume of 0.5 ml/kg/h for 6 hours [7].

This work has been reported in line with the SCARE 2020 criteria [8].

Discussion

Untreated VL is a systemic fatal disease caused by the Leishmania donovani complex. The disease is particularly prevalent in low-income nations such as East Africa and India subcontinent [9].Pentavalent antimonial compounds have been the first-line treatment for VL in different countries since the 1940s [9].In Somalia and East Africa in general, immune-competent people with VL are now treated with sodium stibogluconate and paromomycin in combination [10]. Although treatment with these combinations is considered safe, acute pancreatitis is one of the side effects patients can develop during treatment as of our patient. Despite the fact that kala-azar nephropathy is still poorly understood, renal impairment has been found in this illness in multiple studies [9]. Salgado et al. [10] examined the renal function of 11 visceral leishmaniasis patients in 2003. Five of the patients had macroscopic haematuria, and one had acute nephritic syndrome. A cross-sectional study of 50 people with chronic visceral leishmaniasis was performed, 28% had a reduced GFR. Hypotension and inflammatory glomerular disease were linked to decreased GFR. After using pitressin, 68% of patients had abnormal urinary concentrating capacity.30% had complete distal renal tubular acidosis, whereas 34% had an incomplete type [1].

Because of the inherent disadvantage of being positive in a considerable number of healthy people and being positive for many times after cure, definitive diagnosis of VL cannot be done using simply serological techniques such as ELISA (11). The patient lived in El Barde, a town in the Bakool region with a large pastoral population, where he may have been in contact with the vector.

However, as in this case, a positive serological test combined with typical clinical symptoms and an excellent response to an amphotericin B liposomal course, which is a specific therapy for VL, would raise the likelihood of VL being the definitive diagnosis.

Conclusion

In endemic areas, endemic parasitic infections such as VL and Malaria should be considered as a probable cause of acute kidney injury. Visceral leishmaniasis can present with many forms of clinical pictures, including the complications like acute kidney injury. When VL is properly treated, the renal function test resolves with no sequalae.

Ethical approval

In our institution, Ethical approval is waived from case reports.

Source of funding

None.

Author contribution

Abdirashid Hashi Mohamed- Study concept, data collection and case writing. Ahmed Muhammad Bashir-wrote an introduction, discussion and critically reviewed the case.

Registration of research studies

Name of the registry:

Unique Identifying number or registration ID:

Hyperlink to your specific registration (must be publicly accessible and will be checked):

Consent

Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal on request.

Provenance and peer review

Not commissioned, externally peer-reviewed.

Guarantor

Abdirashid Hashi Mohamed and Ahmed Muhammad Bashir.

Declaration of competing interest

Authors declare no conflict of interest.