You not mention about the Ayurvedic drug name and viral marker however  i think it is a case of AGN with AKI due to viral hepatitis with drug.

I am really worry about the possibility of HUS or TTP. What about the hemogram, liver function, and coagulation profile? The patient is also apparently hypertensive which needs attention. Bless her.

Have you thought about a nephritic syndrome secundary to a leptospirosis (but you would need to research more about the history of jaundice) or a hepatitis

The patient has Edema, hypertension, hematuria, oliguria, and history of sore throat. Makes me think of postestreptococal glomerulonephritis. The jaundice does not fit in this box. It has already disappeared? Presented choluria? It is at the expense of conjugated bilirubin conjugate or not?

based on the symptoms it is related to kidney disease.

most likely we are dealing with acute glomerulonephritis.

INVESTIGATIONS

CBC:    Hb: 5.4 g/dl,

              WBC(TC): 4,500/cmm

              RBC: 1.5×10¹²/L

              Platelet Count: 70,000/cu.mm

              DC: N: 62%       E: 06%

                     L: 30%        M: 02%

MCV: 110 fl, MCH: 29.2 pg, MCHC: 26.5 gm/dl, RDW : 27.5%

PBF:

     RBC: Gross anisopoikilocytosis with microcytic hypochromic cells, few polychromatic cells, fragmented cells, target cell, tear drop cell, occasional microspherocytes, nucleated RBC.

    Comment: Hemolytic anemia with thrombocytopenia

               Urine R/E:  Pus Cell: 1-2/HPF

                  RBC: 25-30/HPF

                  Protein: ++++

Urine C/S:  No growth

S. Creatinine: 9.26 mg/dl

Serum Electrolytes: Na  : 127 mmol/L

                             K    :  6.2 mmol/L

                            Cl    :  100 mmol/L

                            TCO2 : 15 mmol/L 

Blood Urea: 218.6 mg/dl

S. Albumin: 27 g/L

S. ALT: 20 U/L

S.LDH: 2100 U/L

S. Ca: 8.3 mg/dl

Coomb’s test: negative

PT: Normal

APTT: ANA: Negative

Anti ds DNA: 10.5 U/ml (Negative)

C3 : 0.396 g/L (Low)

C4: 0.314 g/L (Normal)

ASO titre: 107 IU/ml

HBsAg- negative

Anti HCV -negative

USG of KUB region:

    Rt Kidney: 9.4 cm;     Lt Kidney: 9.8 cm

    Cortical echogenecity is increased.

    Cortico-medullary differentiation is poor.

    UB: normal Normal

Renal biopsy- Mesangial proliferative glomerulonephritis

Please se the article at below:

Hemolytic-Uremic Syndrome in childhood

To me it looks like HUS but I might be wrong. It is kind of intereting why the MCV so high even with pictures of anisopoikilocytosis with microcytic hypochromic cells. She might need hemodialysis to pull her through the difficulty. However, the cause of it is unknown to me. Have you tried to identify E. coli? I am not a hematology or nephrologist but you should have them involved.

Initially we treated this patient as a rapidly progressive GN with Inj Methylprednisolone 6 dose and Intermittent peritoneal dialysis plus other supportive management like antihypertensive. Blood picture revealed just like HUS and still our differencial diagnosis  is atypical HUS. Now she is on maintenance  hemodialysis and oral prednisolone. Her urine output is only 50 to 100 ml per day and predialytic creatinine is around  4 mg/dl.

Great to learn that her condition is better. There are so many possibilities for HUS and you need to consider some factors that are specific to your locale. It is not uncommon that we end up not able to identify the cause of it but any treatable condition needs to be identified. It seems you have rule out lupus as the cause with negative dsDNA test but other test maybe needed to completely rule it out. The kidney biopsy maybe lupus related. However, her treatment is at this moment adequate in my opinion.

Nice case presentation 

I could not give a sharp final diagnosis, but I have some points:

1-  We can summarize the problems in renal failure and hemolytic anaemia.

2- atypical HUS remains as the most probable diagnosis.

3- This girl mostly has an underlying kidney problem (U/S findings).

4- What about pigmentary nephropathy?

5- Malignancy still has to be excluded.

Obviously with the complete history the aemolyric anemia and renal failure are the main problems,  HUS is the most probable diagnosis, as Dr. Abdelkreem and other quotes.

I'm worried about renal function, because acute kidney injury occurs in 55-70% of patients with typical HUS (Shiga-like toxin–associated HUS [Stx-HUS]) is the classic, primary or epidemic form of HUS, but they have a favorable prognosis, and as many as 70-85% of patients recover renal function, in epidemic HUS. Itá more common at younger ages.

Atypical HUS (non–Stx-HUS) can be sporadic or familial. As the name implies, infection by Stx-producing bacteria is not the cause, and disease may occur year-round without a gastrointestinal prodrome (D-HUS). Overall, patients with non–Stx-HUS have a poor outcome, and as many as 50% may progress to end-stage renal disease (ESRD) or irreversible brain damage. Up to 25% of patients die during the acute phase. The familial form is associated with genetic abnormalities of the complement regulatory proteins.

The clinical response and the evolution of the patient may answer most of these dudes.

Please update us the course of the patient. Thanks for sharing.

At last we discharge the girl as "Atypical Hemolytic Uremic syndrome"

Maintenance  hemodialysis is ongoing.

Thanks everybody for  valuable comments , advice and participation.