Table 1 Description of cases of VL with renal injury and outcome

Age

40

35

24

49

Years since HIV contamination

15

11

24

16

Years since diagnosis of visceral Leishmaniosis

11

9

2

19

Renal syndrome

Nephritic syndrome

Nephrotic syndrome

AKI

Nephrotic syndrome

Biology

Leishmania quantitative PCR test (parasites/ml)

6225 (blood)

1700000 (kidney)

Not available

11570 (blood)

C4 concentration (normal range 0.14-0.33 g/l)

0.12

Not available

0.14

0.2

Cryoglobulin

Positive

Not available

Positive

Positive type 2

HCV serology

Negative

Negative

Negative

Positive

HCV viral load in blood (qualitative)

-

-

-

Negative

Serum albumin (g/l) at time of diagnosis or during follow-up

25

22/14

-

20/24

Plasma hyper-gammaglobulinemia

Yes

Unknown

Yes

Yes

Platelets >150000 giga/L at time of renal biopsy

Yes

Yes

Yes

Yes

Severe clottingdysfunction

No

No

No

No

Hepatic function

Normal

Normal

Normal

Normal

HIV viral load (copies/ml)

162

41000

2000

< 40

CD4 T-cell count (cells/mm ³ )

114

12

70

84

CD4 T-cell nadir (cells/mm ³ )

46

12

50

84

Plasma creatinine concentrations (year, [μmol/l]) diagnosis/follow-up

143/152

2006 (100)/2007 (265)/2008(488)

154 / 99

55 / 60

CKD-EPI (ml/min/1.73 m ² ) diagnosis/follow-up

48/47

105 / 90 / 52

69

Urinalysis

Daily proteinuria (g/day) Diagnosis/follow-up

2.1

1.5/2.0/3.0

0.3 / 0.5

2.0 / 0.5

Hematuria/Leukocyturia

+/-

+/-

-/+

-/-

Kidney histological findings

MPGN III

MPGN III and Interstitial nephropathy

Interstitial nephropathy

MPGN III and interstitial nephropathy

Treatment and outcome

VL treatment regimen

l-Amph-B, Pentamidine

l-Amph-B, Pentamidine,

l-Amph-B

l-Amph-B, Miltéfosime

Miltefosine

Renal outcome

Improved

Not improved

Improved

Improved but worsened at clinical relapse

Patient outcome

Partial recovery

Died

Partial recovery

Died