WHAT IS MEDICINE

THE SCIENCE DEALS WITH

 DIAGNOSIS
 TREATMENT
 PREVENTION OF DISEASE
WHAT IS NEPHROLOGY

BRANCH OF MEDICINE DEALS WITH

 DIAGNOSIS
 TREATMENT
 PREVENTION OF KIDNEY DISEASES
KUB STRUCTURE
KIDNEY CROSS SECTION
GLOMERULUS STRUCTURE
DISEASES OF KIDNEY

 GLOMERULAR DISEASES

 AKI

 CKD
GLOMERULAR DISEASES

 NEPHROTIC SYNDROME

 NEPHRITIC SYNDROME
Nephrotic Syndrome
DR FARYAH
 DEFINATION

Nephrotic syndrome is a clinical syndrome of

 Protein in urine grater than 3.5 g/day

 BODY Oedema

 Hypoalbuminaemia of < 25g/l normal level(34-54g/l)

 Hypercholesterolaemia
 Etiology
Common

Primary or Idiopathic Secondary cause of

(Unknown cause) Nephrotic Syndrome

• MINIMAL CHANGE DISEASE • Post Streptococcal

• FOCAL SEGMENTAL Glomerulonephritis
GLOMERULOSCLEROSIS • Systemic Lupus Erythematous
• MEMBRANOUS NEPHROPATHY
• HSP
• AMYLOIDOSIS
• DIABETIC
GLOMERULONEPHROPATHY
1.MINIMAL CHANGE DISEASE

 THINNING/EFFACEMENT OF PODOCYTES FOOT PROCESSES

 NORMAL GLOMERULI
 MAINLY IN CHILDREN
 EXCELLENT RESPONSE TO STEROIDS
 TRIGERRED BY INFECTION OR LYMPHOMA
2.FSGS(FOCAL SEGMENTAL
GLOMERULOSCLEROSIS)
 MORE COMMON IN AFRICAN-AMERICAN
 CAN BE IDIOPATHIC
 CAN BE DUE TO HIV ,SICKLE CELL,HEROINE ABUSE
 INCONSISTENT RESPONSE TO STEROID
 MAY PROGRESS TO CKD
 LIGHT MICROSCOPY SHOWS SEGMENTAL SCLEROSIS
 EM-EFFACEMENT OF FOOT PROCESSES LIKE MINIMAL CHANGE DISEASE
3.MEMBRANOUS NEPHROPATHY

 CAN BE DUE TO DRUGS(NSAIDS,PENICILLAMINE)

 CAN BE DUE TO INFECTIONS(HBV,HCV),SLE,SYPHILIS OR TUMORS
 POOR RESPONSE TO STEROIDS
 MAY PROGRESS TO CKD
 EM—SPIKE AND DOME APPEARANCE
 LM—DIFFUSE GBM THICKENING
AMYLOIDOSIS

 IT IS A PART OF SYSTEMIC AMYLOIDOSIS

 AMYLOID DEPOSIT IN KIDNEYS(AL OR AA AMYLOID)

 LIGHT MICROSCOPY SHOWS AMYLOID DEPOSIT IN MESANGIUM

DIABETIC GLOMERULO NEPHROPATHY

 IT CAN LEAD TO END STAGE KIDNEY DISEASE

 GLOMERULAR BASEMENT MEMBRANE THICKENING

 GLOMERULOSCLEROSIS
CLINICAL
PRESENTATION
• Periorbital oedema
(earliest sign)
• Scrotal, leg and ankle
oedema
• Ascites
• Breathlessness
 INVESTIGATIONS

Blood
Urine Others
• Renal profile
• Urine C/E • ANA
(RFTs,S/E)
• Urine culture • Anti-dsDNA
• Serum cholesterol
• Quantitative urinary • C3, C4
• Liver function tests-
protein excretion (spot • ASOT
Particularly serum
albumin urine protein:
creatinine ratio or 24
hour urine protein)
 Renal biopsy
Renal biopsy is Not needed prior to corticosteroid / cyclophosphamide therapy because 80% of
children with idiopathic nephrotic syndrome have minimal change steroid responsive disease

Main indication for renal biopsy:

- Steroid resistant nephrotic syndrome
Defined as failure to achieve remission despite 4 weeks of adequate corticosteroid therapy.

- Features that suggest non-minimal change nephrotic syndrome:

Persistent hypertension, renal impairment, and/or gross haematuria
 Management

• FLUID RESTRICTION
• Diet ( normal protein, low salt, adequate calories)
• CORTICOSTEROIDS 4 WEEKS
• CYCLOPHOSPHAMIDE OR CYCLOSPORIN
• Antibiotics ( T. Penicillin V) – initial diagnosis/ relapse
 125 mg BD (1-5 years age)
 250 mg BD (6-12 years)
 500 mg BD (>12 years)
• DIURETICS
• HUMAN ALBUMIN
 Diuretics (e.g. frusemide) – use with caution of hypovolaemia.

 Human albumin (20-25%) at 0.5 - 1.0 g/kg together with IV frusemide at 1-2 mg/kg to
produce a diuresis (can be used in symptomatic grossly oedematous states).

 Fluid restriction - not recommended except in chronic oedematous states.

Remember to monitor BP, hemodynamic status, urine output closely !!!

Assess haemodynamic status
 SYMPTOMS OF Hypovolaemia
o Abdominal pain, cold peripheries, poor
capillary refill, poor pulse volume with or
without low blood pressure
 SYMPTOMS OF Hypervolaemia
o Basal lung crepitations, rhonchi, hepatomegaly,
hypertension.
 General advice
 High probability (85-95%) of relapse.
 Home urine albumin monitoring (once daily, first morning urine).
 To consult the doctor if proteinuria ≥ 2+ for 3 consecutive days, or 3 out of 7 days.
 To consult the doctor if oedematous regardless of the urine dipstick result.
 Immunisation: only killed vaccines is safe while the child is on corticosteroid treatment and
within 6 weeks after its cessation.
 Pneumococcal vaccine should be administered to all children with nephrotic syndrome
(when the child is in remission)
 Corticosteroid therapy
Oral Prednisolone should be started at:
60 mg/ m²/day ( maximum 80 mg / day ) for 4 weeks

40 mg/m²/every alternate morning (EOD) (maximum 60 mg) for 4 weeks

then reduce Prednisolone dose by 25% monthly over next 4 months

(Total 6 months duration of treatment)

 80% of children will achieve remission (defined as urine dipstick trace or nil for 3
consecutive days) within 28 days.

 If fail to achieve response to an initial 4 weeks treatment with prednisolone at 60 mg/m²/

day -> Steroid resistant Nephrotic syndrome -> Refer Paeds nephrologist for renal biopsy
Side effects of corticosteroids
Nephrotic chart

Date Time BP Input Output Balance Weight Urine

protein
COMPLICATION OF NEPHROTIC
SYNDROME
 INFECTION(loss of antibodies)
 THROMBOEMBOLISM(due to loss of antithrombim 111)
 CARDIOVASCULAR COMPLICATIONS
 HYPOVOLEMIC CRISIS
 ANEMIA
 ACUTE RENAL FAILURE
 EDEMA
complications

Complications Clinical Features

• Abdominal pain, cold peripheries, poor pulse volume,
Hypovolemia hypotension, hemoconcentration
Treatment
• Infuse Human Albumin 0.5 to 1.0g/kg/dose fast.
• Human plasma

Infection Clinical Features

Primary Peritonitis • Fever, abdominal pain, tenderness in children within newly
diagnosed or relapse nephrotic syndrome.
Treatment
• Parenteral Penicillin and 3rd generations Cephalosporin

Thrombosis Thorough investigation and adequate treatment with

anticoagulation is usually needed.
Consult nephrologist
 Treatment of steroid dependent nephrotic syndrome

 Defined as ≥ 2 consecutive relapses occurring during steroid taper or within 14 days of the
cessation of steroids.

Treatment
- If the child is not steroid toxic, re-induce with steroids and maintain on as low a dose of
alternate day prednisolone as possible
- If the child is steroid toxic (short stature, striae, cataracts, glaucoma, severe cushingoid
features) consider cyclophosphamide therapy.
 Cyclophosphamide therapy
 Indicated in steroid dependent nephrotic syndrome with signs of steroid toxicity
 Parents should be counselled about the effectiveness and side effects of Cyclophosphamide
therapy
 Leucopenia
 Alopecia
 Haemorrhagic cystitis
 Infertility
 Dose: 2-3 mg/kg/day for 8-12 weeks (cumulative dose 168 mg/kg)
 Monitor full blood count and urinalysis 2 weekly after started
 Relapses post
Consider :
Cyclophosphamide
 Cyclosporine
 Levamisole

To do renal biopsy before initiation, to discuss with paediatric nephrologist

 Steroid resistant nephrotic syndrome
 Refer for renal biopsy.
 Specific treatment will depend on the histopathology.
 General management of the Nephrotic state:

 Control of edema
 Restriction of dietary sodium.
 Diuretics
 Monitor BP and renal profile 1-2 weeks after initiation of ACE
inhibitor or AIIRB
 Control of hypertension (ACE inhibitor/AIIRB).
 Penicillin prophylaxis.
 Nutrition (normal dietary protein content, salt-restricted diet)
 Evaluate calcium and phosphate metabolism.
 Q&A
 Definition of nephrotic syndrome?
 Definition of relapse nephrotic syndrome?
 What is remission?
 Side effects of steroids?
 Complication of nephrotic syndrome?
 SCENARIO

 A 10-yr old child presents with swelling of legs and puffy eyelids. Examination
confirms puffy eyelids and 3+ edema of legs below the knees. BP is normal
 Question: What lab tests will you order?
ANSWER

 ◆ Urinalysis
 ◆ Urine protein to creatinine ratio
 Renal panel
 ◆ Lipid profile
 CBC
 Renal ultrasound
SCENARIO 2

 >Name: Rhythm Rai

 Religion: Hindu
 Age: 2.5 years
 Sex: Male
 • Reported to the pediatric emergency with the chief complains of
Generalized swelling of the body X5 days.
 Swelling started from the face followed by swelling of abdomen, upper and
lower limbs.
 No h/o of rash, fever, sore throat, fast breathing
 Patient was taken to the local hospital and some medicine was given, a USG
was done and referred to BPKIHS.
 DIFFERENTIALS

 MOST LIKELY DIAGNOSIS

SCENARIO 3

 History of Present Illness

 The patient was apparently well 5 days back when his mother noticed
swelling of her face, which was acute in onset and gradually progressing
towards the abdomen and bilateral upper and lower limbs.
 The swelling is painless and pitting in nature.
 ⚫The overlying skin was normal and there is no history of itching and rashes.
 h/o frothy urine ,NO yellowish discoloration of urine
 No h/o cough, chest pain
 No h/o abdominal pain, loss of appetite, vomiting.
 No h/o fever, joint pain, photosensitivity and oral ulcers
 NEPHRITIC SYNDROME
Nephritic syndrome is an inflammatory process that is defined as the presence of one or
more of the following: [1]
 Hematuria

 RBC

 Proteinuria
 (< 3.5 g/24 h)
 Hypertension
 Mild to moderate edema

 Oliguria
Investigations of nephritic

 Urinalysis

 Blood tests

 Renal biopsy
URINALYSIS

Hematuria
Rbcs
Wbcs
Casts
Sterile pyuria
BLOOD TESTS(RFTS,S/E)

 ↑ Creatinine

 , ↓ GFR

 Azotemia

 with ↑ BUN

 Complement, ANA
 , ANCA
 , and anti-GBM antibodies
Renal biopsy

 For non specific disease pattern renal biopsy Is indicated

TREATMENT
1.Supportive therapy

 Low-sodium
 diet
 Water restriction

2.Medical therapy
 Ace Inhibitors,arbs
 Prednisolone,immunosupressants
 Immunosuppresive Therapy
 Plasmapheresis
TYPES OF NEPHRITIC1.Membranoproliferative
glomerulonephritis

: characterized by deposition
of antibodies between podocytes and the
basal membrane

Treatment:steroid ,immunosuppression
with MMF
2.ACUTE POST STREPTOCOCCAL
GLOMERULONEPHRITIS

AFTER GROUP A BETA HEMOLYTIC STREPTOCOCCAL INFECTION

2-4 WEEKS AFTER SORETHROAT
INFLAMMATORY DISEASE
CAUSE INFLAMMATION OF TINY BLOOD VESSELS IN THE FILTERING UNIT OF
KIDNEYS(GLOMERULI)
KIDNEYS UNABLE TO FILTER URINE
COLA COLOURED URINE AND HYPERTENSION
IGG IGM AND C3 DEPOSITION IN ALONG GBM
TREATED WITH ANTIBIOTICS
DIFFUSE PROLIFERATIVE
GLOMERULONEPHRITIS
 SEEN IN AUTOIMMUNE DISEASES(SLE ETC)
 BOTH NEPHRITIC AND NEPHROTIC

 HEMATURIA,PROTEINURIA,HYPERTENSION,RED CELLS IN URINE

 CAUSED BY STREPTOCOCCUS
 IGG AND C3 DEPOSITION IN INTRAMEMBRANOUS AND SUBENDOTHELIAL
RAPIDLY PROGRESSIVE
GLOMERULONEPHRITIS(CRESCENTIC)
 CRESCENT(MOON SHAPE GBM) DUE TO DEPOSITION OF FIBRIN AND PLASMA
PROTEINS

 POOR PROGNOSIS

 TREATMENT:METHYLPREDNISOLONE AND CYTOTOXIC AGENTS

IGA NEPHROPATHY

 BUERGER DISEASE
 HENOSH SCHOELEIN PURPURA
 TRIAD OF HEMATURIA,ABDOMINAL PAIN AND PURPURA
 IGA DEPOSIT IN MESANGIUM

TREATMENT
 MAINLY SUPPORTIVE
 ACE INHIBITORS AND ARBS FOR HYPERTENSION
 RESTRICT SODIUM
 HYDROXYCHLOROQUINE IN PROTEINURIC PATIENTS
1ST scenerio

 A 13-year-old girl with no medical history presented with a week of edema,

malaise and headache. On physical examination there is generalized edema,
BP: 140/95. No skin lesions. No other alterations.
 Paraclinical: Hb: 14 mg/dL, Ht: 41.5%, normal white blood cell count and
platelets. ANA and anti-DNA: negative; C3: 62 mg/dL (90-180), C4: 17 mg/dL
(10-40). Serum creatinine 1.9 mg/dL, BUN 29 mg/dL. Studies for viruses:
negative. Urinalysis: erythrocytes: 20-30/CGA; leukocytes: 6-8/CGA, nitrites
negative, proteinuria 1.7 g/24h.
2.

 Patient is a 70 yrs. old male referred for elevated creatinine and proteinuria
is 2g/day. He has had mildly elevated blood pressures which have been
systolic in the 140-150 range and 80’s for diastolic but more recently in
165/95 range. with a creatinine of around 1.3-1.4 mg/dl. He has history of
dysuria, hematuria, urgency, increased frequency, nocturia. He has foamy
urine. For the past 2-3 months he has been having swelling in his legs. ROS
otherwise negative
3.Urine complete exam finding

 , the urine has greater than 5 RBCs/ HPF along with acanthocytes, dysmorphic
RBCs, and red blood cells (RBCs) casts and in a few cases white blood cells
(WBCs) casts.[18] The hematuria usually is marked with brownish (cola)
colored urine.

 Diagnosis??
diagnosis

 Nephritic syndrome
UTI(URINARY TRACT INFECTION)

 IT IS INFLAMMATION OF URINARY TRACT

BACTERIA ENTER THROUGH URETHRA TO CAUSE INFALMMATION
ALSO CALLED ACUTE BACTERIAL CYSTITIS BECAUSE IT MAINLY AFFECTS BLADDER
(Urinary tract infection (UTI) is a term that is applied to a variety of clinical
conditions ranging from cystitis to severe infection of the kidney with
resultant sepsis)
 UTI

Lower UTI Upper UTI

cystitis Pyelonephritis

60
May also be classified as
1. Isolated UTI
a single episode of lower tract infection occurs
frequently in females and is rarely complicated.
2. Recurrent UTI
is >2 infections in 6 months, or 3 within 12
months.
SYMPTOMS OF UTI

 SUPRAPUBIC PAIN
 DYSURIA(PAIN DURING MICTURATION)
 URINARY FREQUENCY(DESIRE TO URINATE MORE)
 URINARY URGENCY
 HESITANCY(BLADDER DOESNOT GET FULLY EMPTY AFTER MICTURATION)
 Immunosuppression
 Tender lumber region
 fever
RISK FACTORS OF UTI

 FEMALE GENDER(SHORT URETHRA)

 INDWELLING CATHETER
 DIABETES MELLITUS(BLADDER EMPTYING GETS SLOW)
 IMPAIRED BLADDER EMPTYING
 BLADDER OUTFLOW OBSTRUCTION
CAUSES OF UTI

 E COLI(MOST COMMON) GRAM NEGATIVE BACTERIA

 STAPHYLOCOCCUS SAPROPHYTICUS GRAM POSITIVE BACTERIA
 KLEBSILLA GRAM NEGATIVE BACTERIA
 PROTEUS MIRABILIS GRAM NEGATIVE BACILLI BACTERIA
ACUTE CYSTITIS

 urinary infection of the lower urinary tract, principally the bladder.

 The diagnosis is made clinically.

INVESTIGATION OF ACUTE CYSTITIS

 Urinalysis WBCs in the urine & hematuria

may be present.
 Urine culture is required to confirm the diagnosis & identify the causative
organism.
 However, when the clinical picture & urinalysis are suggestive of the Dx of
acute cystitis, urine culture may not be needed.
TREATMENT OF ACUTE CYSTITIS

 Management for acute cystitis consists of a short

course of oral antibiotics.
TMP SMX
Nitrofurantoin
Quinolones(CIPRO,LEVOFLOXacin)
Short oral course 3-5 d ♀
Days for ♂& child 7 d
GENERAL TREATMENT

 FLOROQUINOLONES Eg CIPRO 20MG/KG/DAY BD FOR 5 DAYS

 CITRALKA SYRUP DECREASES URINE PH
 CRANBERRY SATCHET PREVENT BACTERIAL ADHESION TO BLADDER WALLS
RECURRENT UTI

Bacterial persistence
presence of bacteria within a site in the urinary tract, leads to repeat episodes
of infection.
 Such sites include
 urolithiasis anywhere in the urinary tract,
 chronic bacterial prostatitis,
 obstructed or atrophic kidney
TREATMENT

 Nitrofurantoin, 50 or 100 mg daily

 TMP-SMX, 40/200 mg daily
 Trimethoprim, 100 mg daily
 Cephalexin, 250 mg daily
 Ciprofloxacin, 250 mg daily
AKI

 ACUTE KIDNEY INJURY

 LEADS TO INCREASE IN CREATININE
 DECREASE IN URINE OUTPUT
 REVERSIBLE IF TREATED ON TIME
DEFINATION

 Acute kidney injury (AKI) is a clinical syndrome manifested by a rapid or

abrupt decline in kidney function and subsequent dysregulation of the body
electrolytes and volume, and abnormal retention of nitrogenous waste. The
widely accepted Kidney Disease: Improving Global Outcome (KDIGO)
definition of AKI is based on the change of serum creatinine and urine output,
as follows [1] :
 Rise in serum creatinine ≥0.3 mg/dL within 48 hours
STAGES OF AKI

 STAGE 1: CREATININE RAISE 1.5-2 FOLD FROM BASELINE

URINE OUTPUT:LESS THAN 0.5ML/KG/HOUR FOR MORE THAN 6 HOURS

 STAGE 2: 2-3 FOLD

URINE OUTPUT:LESS THAN 0.5ML/KG/HOUR FOR MORE THAN 12 HOURS

 STAGE 3:GREATER THAN 3 FOLD INCREASE IN CR FROM BASELINE

 URINE OUTPUT:LESS THAN 0.3ML/KG/HOUR FOR MORE THAN 24 HOURS
Phases of AKI

 What are the 3 phases of acute kidney injury?

 Types and phases of AKI
 Onset phase: Kidney injury occurs.
 Oliguric (anuric) phase: Urine output decreases from renal tubule damage.
 Diuretic phase: The kidneys try to heal and urine output increases, but tubule
scarring and damage occur.
 Recovery phase: Tubular edema resolves and renal function improves.
 CAUSES OF AKI
 PRE RENAL 1.SYSTEMIC 2.LOCAL
HEMORHAGE RENAL ARTERY STENOSIS
HYPOTENSION
SEPSIS

 RENAL
PARENCHYMAL DISEASE
TOXICITY
DRUGS
GLOMERULAR

 POST RENAL
OBSTRUCTION
STONE
TUMOR
FEATURES/SYMPTOMS

 INCREASE UREA,CREATININE
 DECREASE IN URINE OUTPUT
 INCREASE IN K
 METABOLLIC ACIDOSIS
 HYPOCALCEMIA
 HYPERPHOSPHATEMIA
 SOB DUE TO FLUID OVERLOAD
ASSESS

 FLUID BALANCE
BP
URINE NOUTPUT

 CHEST
 BLADDER
INVESTIGATIONS

 BLOOD TESTS CHEST XRAY

 RENAL PANEL(RFTS,S/E) ECG(TALL T WAVES IN HYPERKALEMIA)
 CALCIUM,PHOSPHATE
 ALBUMIN
 CRP
 CLOTTING SCREEN
 ABGS/VBGS
 USG
 URINE COMPLETE
MANAGEMENT

 TREAT UNDERLYING CAUSE

 TREAT HYPOVOLEMIA(BLOOD,PLASMA,SALINE)
 CORRECT METABOLLIC ACIDOSIS
 SODIUM BICARBONATE TO CORRECT METABOLLIC ACIDOSIS
 TREAT HYPERKALEMIA
 DIALYSIS
ATN(ACUTE TUBULAR NECROSIS)

 IT IS ACUTE NECROSIS OF RENAL TUBULAR CELLS

 CAUSES:ISCHEMIA,NEPHROTOXICITY,BACTERIA,DRUGS(GENTAMYCIN,AMPHOTERICIN B)
 DEAD TUBULAR CELLS CELLS SHED INTO TUBULAR LUMEN LEADS TO OBSTRUCTION OF
TUBULE
 IT CAN BE REVERSIBLE BCZ TUBULAR CELLS CAN REGENERATE IF TREATED ON TIME
ATN TREATMENT

 TREAT CAUSE
 RESTORE RENAL PERFUSION
 AVOID NSAIDS
 AVOID NEPHROTOXIC DRUGS
 TREAT INFECTIONS
CKD(CHRONIC KIDNEY DISEASE)

 IRREVERSIBLE DAMAGE TO KIDNEYS DEVELOPS OVER YEARS

 STRUCTURALLY OR FUNCTIONALLY
 LOSS OF KIDNEYS FUNCTION WHICH ARE EXCRETORY,ENDOCRINE,METABOLLIC
STAGES OF CKG

 STAGE 1
GFR GREATER THAN 90,MILD,ASYMPTOMATIC
 STAGE 2
GFR 60-90,MODERATE,ASYMPTOMATIC
 STAGE 3
GFR 30-60,USUALLY ASYMPTOMATIC,ANEMIA
 STAGE 4
GFR 15-30,SYMPTOMATIC,EKLECTROLYTR PROBLEMS
 STAGE 5
GFR LESS THAN 15,COMPLICATIONS,DIALYSIS
INVESTIGATIONS OF CKD

 RFTS
 S/E
 SERUM CA,P,PTH
 URINALYSIS
 ALBUMIN
 CBC
 HBA1C
 USG KUB
 VIRAL MARKERS
 ECG
MANAGEMENT OF CKD

 Control your blood pressure.

 Meet your blood glucose goal if you have diabetes.
 Work with your health care team to monitor your kidney health.
 Take medicines as prescribed.
 Work with a dietitian to develop a meal plan.
 Make physical activity part of your routine.
 Aim for a healthy weight.
TREATMENT

 CAP OMEPRAZOLE
 TAB QALSAN D
 TAB F/S
 ANTIHYPERTENSIVE
 INJ ERYTHROPOITIN
 ANTIDIABETIC REGIME
 TAB SODAMINT
 TAB LOPHOS
ESRD
CAUSES OF ESRD