Renal-type edema was the most common reason.

Here are the other reasons for consultation (Table 4).

Sixty-one patients, or 38.60%, had their weight reported in the files. The average weight was 70.95 ± 10.79 kg.

The mean diuresis was 1550 ± 569.97 ml/24h with extremes of 0 to 3000 ml/24h. And the patients had normal diuresis in 74.1%. The diuresis parameters are shown below.

Patients had normal blood pressure in 51.9%. The average SBP was 130.5 ± 8.5 mm hg and that of the DBP was 77.27 ± 9 mm hg. Eighty-nine patients had hypertension, i.e. 56.32%, see Table 5 below.

The average hemoglobin was 11.05 ± 2.63 g/dl and the extremes 5.1 g/dl and 17 g/dl. Fifty-eight patients were anemic, i.e. 36.7%.

Mean albuminemia was 19.09 ± 9.14 g/l with extremes of 2 and 47 g/l.

Eighty-one people had hypoalbuminemia, i.e. 51.26%.

The mean protein level was 50.84 ± 11.94 g/l with extremes of 30 and 83 g/l.

Seventy-five people had hypoprotidemia, i.e. 47.46%.

The average urea was 0.70 ± 0.83 g/l. And the extremes of 0.11 and 4.93 g/l. 49 people had hyperuremia, i.e. 31.01%.

Mean serum creatinine was 33.74 ± 51.69 mg/l, and extremes from 4 to 394 mg/l. And ninety-six people had impaired kidney function, or 61%. And Figure 2 below represents a distribution of patients by stage of kidney disease.

Mean serum calcium was 80 ± 13.06 mg/l with extremes of 60 and 95 mg/l. Ten people had dosed serum calcium, i.e. 6.32%.

The mean HDL cholesterol was 0.37 ±0.13 g/l with extremes of 0.21 and 0.57 g/l.

The average LDL cholesterol was 3.02 ± 1.5 g/l with extremes of 0.83 and 5.04 g/l.

Fifty-three patients or 33.54% had retroviral serology among which one patient or 1.88% had positive serology and the other patients (52) or 98.11% had negative serology.

Forty-seven patients or 29.74% had done the AgHbs and 4 patients or 8.51% or had the AgHbs positive.

Thirty-seven patients or 23.41% had anti-HCV Ab and one patient or 3.7 had positive anti-HCV Ab.

The average of 24-hour proteinuria (PU/24 hours) was 6.4 ± 3.69 g/24 hours, and the extreme was from 0.37 to 18.50 g/24h. The median was 5.9 g/24h. Patients had nephrotic proteinuria in 84.86%.

Proteinuria according to slices is shown below (Table 6).

Forty-one patients or 25.94% underwent HLM, among which 10 patients or 24.39% had hematuria and 18 patients or 43.9% had leukocyturia.

Kidney size

In 88.74% of cases, kidney size was normal.

The following is the representation according to the size of the kidneys of the patients (Table 7).

Histological types

Non-specific FSGS or NOS (Not Other Specificities) was found in 62 cases or 39.24%, collapsing FSGS in 48 cases or 30.40%, 6 cases of tubular TIP FSGS or 3.79%, 5 cases of cellular FSGS i.e. 3.16% and 2 cases of vascular or hilar FSGS i.e. 3.16%.

Figures 3-7 below represent the histological types of FSGS.

Tubulointerstitial and vascular repercussions.

Patients had no tubulointerstitial and vascular repercussions in 76% of cases.

Figure 8 represents the percentage of tubulointerstitial and vascular impact.

Specifically, the types of vascular repercussions have been grouped together in Table 8.

Immunofluorescence was performed in 13 patients confers Table 9.

Among the 158 cases of FSGS collected, 123 cases were primary (77.17%) and 35 cases had an etiology, 22.83%. See Table 10 of causes.

· Lifestyle and dietary measure

All the patients benefited from lifestyle and dietary measures.

· Nephroprotective treatment

Of the 158 patients, 133 patients or 84.17% received nephroprotective treatment with IEC and ARA2.

· Diuretics

Of the 158 patients, ninety patients or 56.9% were treated with diuretics. Eighty-two patients or 91.1% were treated with loop diuretics alone, then 4 patients or 4.4% were treated with dual diuretics; loop diuretic plus either a potassium-sparing diuretic or a thiazide diuretic.

· Etiological treatment.

For patients with secondary HSF, the treatment was etiological.

For primary FSGS out of the 158 patients collected for FSGS, 103 received immunosuppressive treatment, i.e. 65.18%. Of these 103 patients who received treatment with immunosuppressants; 95 patients received corticosteroid therapy alone, i.e. 92.23%, 7 patients, i.e. 6.8% due to corticosteroid dependence or corticoresistance, received corticosteroid therapy combined with another immunosuppressant. This immunosuppressive treatment used was either azathioprine in 4.8% (5 patients), or cyclophosphamide in 2% (2 patients). One patient, or 0.97%, had received the 3 immunosuppressants (cyclophosphamide, azathioprine, mycophenolate mofetil) during follow-up at different times (See Table 11).

Corticosteroid therapy was prescribed at a dose of 1 mg/kg/day for an average of 2.8 months in all patients.

Azathioprine was prescribed at a dose of 50 mg twice daily for an average of 11.6 months.

Mycophenolate mofetil was prescribed at a dose of 1 g twice a day for an average of 6 months and cyclophosphamide was prescribed at a dose of 500 mg per square meter for an average of 6 months.

The evolution under treatment for twelve months was marked by 12 cases or 7.59% of corticoresistance, 15 cases or 9.49% of corticosensitivity and 4 cases or 2.53% of corticodependence.

Nineteen patients put on hemodialysis and peritoneal dialysis.

The complications found were: one case of corticosteroid-induced diabetes, one case of femoral neck fracture, 4 cases of urinary infections, 3 cases of skin infections and 1 case of digestive infection.

The P-Value was significant for sex, age and hypertension.

The anamnestic and clinical data correlated to the types of FSGS are shown below (Table 12).

The P-Value was significant for serum creatinine and 24-hour proteinuria. See Table 13.

P-values were significant for dedifferentiation, vascular lesions, and tubulointerstitial lesions. The sonographic and histological data correlated to the types of FSGS are shown below (Table 14).

P-values were not significant for all parameters. See Table 15 below.

The first reason for hospitalization found was edema, i.e. 93.3%, this was identical to the work of Van Rensburg BWJ et al. in South Africa and Narasimhan B et al. in India [3] [10] .

In 82.91% of cases the diuresis was normal. This is corroborated by the work of Haas et al., Weiss et al., and Detwiler et al. [8] [12] [13] in which diuresis was normal in 80% of cases.

And 56.1% of patients had normal blood pressure either less than or equal to 120/80mmhg.

However 8.3% of patients with collapsing HSF had hypertension. The P-Value was 0.008 or p < 0.01 or significant. This was corroborated with the work of Haas et al. [8] , Weiss et al., and Detwiler et al. [12] [13] .

The prevalence of segmental and focal hyalinosis listed was 158 cases with 123 primary cases or 77.17% and 35 cases with etiology or 22.83%. Among the primary cases, the NOS FSGS type is the most represented 62 cases or 39.24% followed by the collapsing FSGS 48 cases or 30.37%.

FSGS with etiology was associated with fibrosis in 5/35 cases, i.e. 1 case out of 7.

The collapsing FSGSs had tubulointerstitial lesions in 66.66% and P 0.006 which is statistically significant.

The 62.5% of the collapsing FSGSs had vascular lesions with 0.35 (0.15 - 0.78) and P 0.01 statistically significant.

Weiss et al. as well as Detwiler et al. had previously shown that collapsing FSGSs were more likely to cause tubulointerstitial lesions [17] [19] .

Tubulointerstitial lesions best correlate with the degree of reduction in glomerular filtration rate (GFR) sign severity.

These tubulointerstitial lesions may be a consequence of glomerular injury through disruption of postglomerular circulation, trafficking of tubular proteins with promotion of local cytokine and growth factor, production of inflammatory infiltrates and promotion of fibrogen or again, the formation of obstructions.

TIP FSGS were the most corticosensitive 33.33% followed by NOS FSGS 11.29% and collapsing FSGS.

There was complete remission in 50% for TIP FSGS and 11.29% for NOS FSGS and 2.08% for collapsing FSGS and no complete or partial remission for vascular and cellular FSGS. The work of Dial et al. [5] had found 29.7% complete remission for the primary forms. In our work we specified the evolution of each type of FSGS that can explain the difference.

Corticoresistance was present in 12.5% of cases of collapsing FSGS versus 8.02% in NOS type FSGS. The other primitive types had no cases of corticoresistance. Steroid dependence was present in 4.83% of cases of NOS type FSGS and in 4.16% of collapsing FSGS. The other types of primary FSGS and secondary FSGS had no cases of corticodependency. This was corroborated by the work of Haas et al. [8] , Weiss et al. as well as Detwiler et al. [12] [13] who found collapsing FSGS to be more corticoresistant.

The complications found were: one case of corticosteroid-induced diabetes, one case of femoral neck fracture, 4 cases of urinary infections, 3 cases of skin infections and 1 case of digestive infection, i.e. 16.66%. MENDOZA et al. [16] had also found 17% of cases of infections in the patients followed.

The evolution of the FSGS in our work reveals that every 8 months the proteinuria decreases by half. Similarly, complete remissions were observed in 8 months in PEI et al. [20] .

Actually, the efficacy of extracorporeal plasma therapy for adult patients with native kidneys with primary FSGS is established. The repeated administrations of retuximab were not associated with an habituation effect and resulted in a high percentage of complete or partial remission comparable to larger pediatric studies. Renal function remained stable during the treatment period. This approach led to an extension of relapse-free survival compared to previous treatment regimens over a median duration of follow-up of 110 months. And the translational study has identified clopidogrel as a promising therapeutic option for FSGS via network-based bioinformatics analysis. Clopidogrel significantly improved key outcome parameters in the adriamycin FSGS mouse model, including albuminuria, weight loss, and histopathological lesions of the kidney. These data, along with a favorable drug safety profile, endorse clopidogrel as an attractive candidate for drug repositioning and subsequent clinical trial evaluation for patients suffering from FSGS [20] [21] [22] .