3 Presenting Complaints A 25 year old male presented in the ER withShortness of breath------>1 day2. Oliguria >1-2 days3. Body swellings >2 months
4 History of Presenting Ilness Shortness of breath initially with exertion, later on developed with lying down also. Also developed cough on lying down.Had oliguria for 1 day, with very small amount of urine eveyday despite adquate intake, no hematuria, no dysuria.Body swellings developed gradually over 2 months, initially over hands and feet, later on extened to elbows and knees resepectively.
5 No hemoptysis, no chest pain, no h/o palpitations, no h/o wheeze. No h/o flank painPatient developed abdominal distention and complained of fullness.No h/o malena, hematemesis, fits, or unconsciousness
6 No h/ joint pains or skin rash. No h/o sore throat preceding these events.
7 Past HistoryNon-hypertensive, non diabetic, non-asthmatic, no cardiac issue in the past.Was diagnosed with Pulmonary T.B 2 years back, took ATT for 9 months.Was not taking any medication, allopathic or homeopathic, prior to these events. And did not take any medication in the past.
8 Personal and Family History Non smoker and has no addiction, be it I/V, snorting or sniffingIs a student by occupation.Has 2 healthy brothers, and 3 healthy sisters, no one has ever suffered from such ailment.Parents are both healthy and do not have chronic disease
9 General Physical ExamA young man of average built with a puffy face and swollen limbs, with an IV line in his right forearm, lying propped up in bed, and is drowsy.Vital Signs:B.P: 140/70Pulse: 100/min, regular.Temp: AfebrileR/R: 20/min
10 General Exam:Jaundice: -Pallor: ++Cyanosis: -Clubbing: -Pedal Edema: +++ ( Pitting, and extending above shins,while both upper limbs are also have pitting edema ) JVP: Not raisedNail infarcts: -Rash: -Lymph Nodes: No nodes palpable throughout the body.No prick marks seen on limbsNeck Veins: Distended
12 Cardiovascular Exam No obvious deformity of Precodium Apex Beat in left 5th ICS 2 cm medial to midclavicular line. Normal character of apex beat.S1+S2+0Heart sounds of normal intensity, no murmur heard.
13 Gastrointestinal Exam Abdomen distended, with fullness in flanks, and a slit like umbilicus.Fluid Thrill + ( Ascites )Liver upper border percussed in right 5th ICS.Lower border not palpated by dipping method.Spleen impalpableKidneys not palpable.Bowel Sounds audible, normal frequency.
14 Respiratory Exam Chest has no obvious deformity Chest movements bilaterally symmetricalFine inspiratory crepts in both lungs extending upto midzonesBreath sounds reduced on right base.
15 ENT EXAMPalatine tonsils not enlarged, no hyperemia or exudates seen on tonsils and post-pharyngeal wall.No Faucial flare.
25 USG ABDOMEN PELVIS: 14 cm liver, normal echotexture Spleen 11.5 cm Both Kidneys upto 14 cm in size, swollen with increased parenchymal echogenecityGross ascitesNo abdominal lymph nodes enlarged
26 USG GUIDED RENAL BIOPSY: SHOWED PROLIFERATIVE CHANGES IN THE ENDOTHELIUM, EPITHELIUM AND TO SOME EXTENT IN THE MESANGIUM IN ALMOST ALL THE GLOMERULI UNDER LIGHT MICROSCOPYDIFFUSE PROLIFERATIVE GLOMERULONEPHRITIS
27 DIFFUSE PROLIFERATIVE GLOMERULONEPHRITIS NORMAL GLOMERULUSDIFFUSEPROLIFERATIVE
28 FINAL DIAGNOSIS ACUTE ON CHRONIC RENAL FALIURE DUE TO NEPHROTIC SYNDROME( DIFFUSE PROLIFERATIVE GLOMERULONEPHRITIS )
29 WHAT IS NEPHROTIC SYNDROME? A SYNDROME CONSISTING OF:PROTEINURIA >3.5 gms/3.75 m²PERIPHERAL EDEMAHYPOALBUMINEMIA <3g/dlCasued by glomerulonephritis which may:DIVIDED INTO:PRIMARY ( IDIOPATHIC )SECONDARY:
30 KEY PROBLEMS IN NEPHROTIC SYNDROME PROTEINURIA:Causes hyperfilteration injury to glomeruliACE inhibitors have a role in reducing proteinuriaPROTEIN RESTRICTION when gfr falls below 25 ml/minINFECTIONS:Due to immunoglobulin loss in urine
31 HYPERCOAGULABLE STATE: Due to HyperlipidemiasUrinary loss of anithrombin IIIIncreased stickiness of plateletsHypercoagulable especially with S/Albumin below 2 g/dlEDEMA:Salt water restriction is required
32 GLOMERULONEPHRITIS PROLIFERATIVE: DIVIDED INTO ENDOCAPILLARY TYPE EXTRACAPILLARY TYPEMESANGIALDIFFUSE PROLIFERATIVE AFFECTS ALL OF THE ABOVESYSTEMIC DISEASES CAUSING THIS ARE:SLEPOST-SREPTOCOCCALIgA NEPHROPATHYCRYOGLOBULINEMIC RENAL DISEASE
33 IN OUR CASE, THE CAUSE COULD NOT BE FOUND, LABLLED TO BE THE IDIOPATHIC TYPE
34 MANAGEMENTHi dose i/v diuretics for peripheral edema and fluid overload if presentSalt water restriction and protein restriction to some extentTreat the systemic disease if presentAnticoagulation prophylacticallyDialysis is rarely required, renal functions improve with treatment of systemic disease or when managed conservatively if is of the idiopathic varietyProteinuria or hematuria ( if nephritic syndrome ) may persist and tendency to develop CKD increases
35 STEROID THERAPY: IMMUNOSUPPRESSANTS: PULSE THERAPY: 1g/day methylprednisolone for 3 days, then 1mg/kg for 4-6 weeks5-10 mg/kg for 6 monthsAlternative is predniosolone 1mg/kg for 6 months not exceeding 80 mg/dayIMMUNOSUPPRESSANTS:Mycofenolate mofetil can be usd in refractory cases.
36 BRIEFLY ABOUT OTHER GLOMERULONEPHRITIDIES MINIMAL CHANGE DISEASE:Most common type in children, and most steroid responsive typeNo changes on light microscopy in glomeruliREMISSIONS RELAPSES AND RESPONSESUPTO 80 percent show remission with steroidsDOSE: DAILY 60 mg or ALTERNATE DAY 120mg/daySteroid dependant and non responders are treated with cyclophosphamide or cyclosporin
37 MEMBRANOUS GLOMERULONEHPRITIS: Commonest type in adultsCauses can be due to drugs, infections and certain tumorsSpontaneous remissions in precentResults of Steroid therapy are conflicting, those with heavy proteinuria benefit more from steroidsCyclophosphamide can be used in steroid non responders
38 MEMBRANOPROLIFERATIVE: Is an uncommon typeDisease of children and young adultsEtiology includes infectious agents i.e Hep C and autoimmmunity i.e SLETreatment with steroids and immunosupressants have not revealed good results in adultsSteroids may prove effective in childrenu
39 FOCAL SEGMENTAL: Associated with HIV and HEROIN abuse There is progressive proteinuria decline in GFRVery less chances of spontaneous remissionTreatments is with steroids and intensive courses of immunosupressants
40 PROGRESS DURING MANAGEMENT With symptomatic treatment, his urine output became adequateThe anasarca gradually improvedHis S/Creatinine came down to 4 mg/dl and urea to below 180 mg/dlBut he developed produtive cough and a massive loculated right sided pleural effusion, along with feverTLC of 20,000 and neutrophilia
41 Pleural tap was hemorrhagic and its examination is as follows: Glucose: 150 mg/dlProtein: 2.5 g/dlLDH: 70 u/lRBCS: 50,000 /cmmWBCS: 2040 /cmmNEUTROPHILS: 80 %LYMPHOCYTES: 20%NO AFB OR MICRO-ORGANISM SEEN