PEDIATRIC NEPHOLOGY MODULE - PowerPoint Presentation

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PEDIATRIC NEPHOLOGY MODULE

6th YearMedical school

Dr.

Reham

Almardini

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Outline

Introduction HematuriaProteinuriaTubulopathy

HUS

Acute Kidney Injury

CKD

RRT

Urology- UTI

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Introduction

Retroperitoneal space Above the level of the umbilicus6 cm, 24 g in term newborn - ≥12 cm, 150 g in an adult

Each kidney contains around 1 million nephrons ( 200000- 1 million)

Number of nephrons completes at 36-40

wk

Functional maturation; continues during the 1st decade of life

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Nephrons Number

New nephrons cannot be formed after birthdiseases results in loss of nephrons lead to renal insufficiency Low birthweight & Prematurity or others Risk factor for: HT, CKD

Low nephron number: hyperfiltration and eventual sclerosis of “overworked” nephron units

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Functions of the kidneys

Filtration and excretion of fluid &waste products Bp. controlAcid base balance Production of Erythropoietin and renin

Activation of vitamin D

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Hematuria

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Definitions Of Microscopic Hematuria

> 5 RBCs/ Mcl of uncentrifuged urine

5- 10 RBC / HPF for resuspended urine sediment

Urine dipstick detects hematuria: Hemoglobin catalyzes an oxidation reaction between

hydrogen peroxide

&

tetramethylbenzidine

impregnated on the dipstick, color change from yellow to green-blue

Other oxidizing agents (free

Hb

and myoglobin) can cause color change in the absence of red blood cells, providing false positive results

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False positive: Hemoglobin, myoglobin, oxidizing agent as hypochlorite, UTI- microbial peroxidases

False negative; reducing substances as Ascorbic acids, high specific gravity

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Hemoglobinuria # Myoglobinuria

Cola colored urine

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Rhabdomyolysis

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Incidence of Hematuria

MaH in a general pediatric population is 0.13% Persistent MiH

occurs in 0.5%-2% of children, varying with definitions of ‘persistent’ and ‘hematuria’

If present on more than 3 occasions over 3 weeks, it is termed

‘persistent’

and requires further investigation

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Causes of Hematuria in the Newborn

Renal Vein thrombosis (Asphyxia, Dehydration, shock)Renal Artery thrombosisAutosomal recessive polycystic kidney disease

Obstructive uropathy

Urinary tract infection

Bleeding and clotting disorder

Trauma, Bladder catheterization

Cortical necrosis (hypoxic/ ischemic perinatal insult)

Nephrocalcinosis (Furosemide in premature)

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Gross hematuria

Majority, 56% have an easily recognizable and apparent causeThe most-common diagnoses assigned were UTI (26%)

Adenoviruses Cystitis, a known etiology of acute hemorrhagic cystitis in children

The common association between gross hematuria and idiopathic

hypercalciuria

and hyperuricosuria has become more apparent

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Causes of recurrent gross hematuria

IgA nephropathyFamilial benign hematuriaAlport Syndrome

Nutcracker syndrome

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In all children with hematuria or proteinuria a clinical evaluation should include blood pressure measurement compared to a reference of normal values for the child’s gender and height

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Features suggestive of renal disease requiring urgent investigation

Fluid overload, Edema, Ascites, Oligoanuria Hypertension

significant proteinuria

Systemic symptoms: joint pain or swelling, Vasculitis rash

previous episodes and significant past medical history such as recent upper respiratory tract infection

Growth impairment

Hearing abnormalities

The presence of a family history of hematuria, renal disease or hearing impairment suggests a familial cause

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Glomerular

Lower Urinary Tract

A brownish-red or ‘cola-colored’

Signs Of GN; HT, fluid overload Absence does not exclude GN

Dysmorphic RBC

Glomerular bleeding alone will not cause a drop in the serum

haemoglobin

.

Anaemia

;

haemolysis

, CRF or heavy LUT bleeding

Red or burgundy

Contain blood clots

Early stream suggests a urethral focus

Terminal stream suggests a bladder focus (e.g. cystitis, calculus, schistosomiasis).

Pain is more suggestive of a LUT source

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Glomerular Causes

PIGN: Common cause of childhood glomerulonephritis; usually managed in a general pediatric inpatient setting

A personal or family history of

MiH

and intermittent gross

hematuriacoinciding

or within days of intercurrent infections is characteristic of IgA nephropathy

IgA nephropathy may present with

MiH

, proteinuria or signs of GN. A raised serum IgA is sensitive but not specific

Henoch

Schonlein

Purpura (HSP) Nephritis is preceded by a history of abdominal pain, bloody stools,

vasculitic

rash and arthritis

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Glomerular Causes

SLE Nephritis: arthritis, polymorphic rash, weight loss, mouth ulcers, malaise, lethargy or cytopenias

.

low C3, C4,

immunoglobulins, raised ANA or ds-DNA antibody

titres

. - A

vasculitic

rash not typical of HSP should prompt testing for SLE and other systemic

vasculitides

via anti-neutrophil cytoplasmic antibodies (ANCA)

HUS: preceded by a diarrhea. hemolytic anemia, thrombocytopenia, and acute renal impairment. Diagnosis is confirmed by stool culture and serology for

E. coli

O157, the most common causative organism in the UK.

Haemoptysis

suggests the rare diagnosis of Goodpasture’s Syndrome, confirmed by anti-GBM antibody

titres

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Alport’s syndrome and Thin Basement Membrane Nephropathy

Inherited glomerulopathies that can present with persistent

MiH

and recurrent

MaH

Historical features supporting Alport’s include a personal or family history of hearing loss, ectopia

lentis

or chronic renal failure

Thin Basement Membrane Nephropathy is supported by

MiH

in well immediate family members and no history consistent with IgA nephropathy or Alport’s syndrome. Diagnosis of thin GBM requires renal biopsy though this is rarely performed

Genetic studies; COL4 mutations

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History

Timing related to URTITraumaRelation to exercise Passage of stone

History of skin infection

Drug intake as calcium or

vit

D

Associated symptoms as urinary ( dysuria frequency urgency), skin rash, joint swelling, fever, face and leg swelling

Presences of other diseases as sickle,

Family history of HT stone deafness renal failure dialysis or transplantation

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Investigation

Step I Confirm the presence of hematuriaStep II; determine site of hematuriaKFT, the presence of proteinuria, S albuminC3 ASOT ANA anti DNAs

Plan

Abdomin

, US, CT

Renal Doppler, MRA

Cystoscopy

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Investigation

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If the microscopic hematuria persists unchanged for more than 1–2 years further evaluation is recommended

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Indication of kidney biopsy

Association with significant proteinuriaPersistent low C3 ( more than 8 weeks)Association of unexplained Azotemia

Systemic manifestation WITH proteinuria suggestive of SLE, HSP

Family history of kidney disease ( ESRF or CKD)

Recurrent gross hematuria of unknown etiology

Anxious parents

Persistence of hematuria more than 2 years

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Questions

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Hemolytic-Uremic

Syndrom

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Hemolytic-Uremic Syndrome

Microangiopathic hemolytic anemiaThrombocytopeniaRenal insufficiency

Etiology

D+ HUS:

Shigella

dysenteriae

type 1 , E. coli O157:H7, E. coli O104:H

neuraminidase-producing

Streptococcus pneumoniae

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Hemolytic-Uremic Syndrome

D Neg HUS

Genetic: factor H deficiency, membrane cofactor protein (CD46) abnormalities , factor 1 deficiency , factor B mutation, C3 mutations

Acquired anti-C3 AB

Immune-mediated factor H deficiency

ADAMTS13  abnormalities

Infectious: HIV

Antiphospholipid syndrome

Lupus, Scleroderma, Malignant hypertension, Malignancy, Pregnancy

Mitomycin

Quinidine

Ticlopidine

Clopidogrel

Calcineurin inhibitors Oral contraception

Deficiency in cobalamin C

Transplant-associated TMA

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Prognosis HUS

Early recognition, intensive supportive caremortality D+ HUS is <5% inDialysis in half of pt

5% dialysis dependent

30% CKD

Pneumococci associated 20% mortality

The familial and the genetic; progressive or relapsing, poor prognosis and recurrence

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Treatment

D+ HUS: SupportivePneumoccocal; Prompt disease treatement

, washed RBC

Plasma therapy in genetic , ADAMST13

Eculizumab

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Idiopathic Hypercalciuria

Autosomal dominant disorderRecurrent gross hematuria, persistent microscopic hematuria, dysuria, or abdominal pain in the absence of stone formationSecondary Hypercalciuria:

hyperparathyroidism, vitamin D intoxication, immobilization, and sarcoidosis

Cushing syndrome, corticosteroid therapy, tubular dysfunction secondary to

Fanconi

syndrome (Wilson disease,

oculocerebrorenal

syndrome), Williams syndrome, distal RTA, or Bartter, Dent disease

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Hypercalciuria

DIAGNOSIS 24 hr urinary calcium excretion >4 mg/kg

Spot Ca/Cr (mg/

dL

: mg/

dL

) >0.2

0.8 in infants <7

mo

of age

Morbidity

: Hematuria, stone, UTI, decrease bone mineral density

Treatment

: high water intake, low sodium diet,

hydrochlorothiazid

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Proteinuria

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Children: Proteinuria > 4 mg/m2/

hr

Nephrotic Range

protienuria

Urine Analysis+3 or +4 or protein/creatinine > 2

24

hr

urine collection ≥ 40mg/m2/

hr

or ≥ 50mg/kg/

hr

Selective proteinuria: only intermediate sized ( less 1000 Da as Albumin, Transferrin)

Non-Selective proteinuria: leak of different protein size including larger- Immunoglobulins

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False Positive Dipstick

Very Alkaline Urine- some UTIHematuria

Very concentrated urine( SG> 1.030)

Chlorohexidine

Contamination

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Causes of proteinuria

Non Pathological causesOrthostatic

Febrile

Exercise induced

Pathological Causes

Tubular (Allergic interstitial nephritis, ATN)

Glomerular ( NS, GN)

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Nephrotic Syndrome

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Clinical presentation

Edema, periorbital, morningAntecedent infection, URTI

Decreased Urine output - frothy or foamy

Abdominal pain

Headache with neurological signs or irritability- should raise the suspicion for

cerebral venous sinus thrombosis

Hematuria (Gross in < 5%, microscopic in 20%)

Hypertension (5%)

2 to 10yrs of age with male predominance(2:1)

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Differential Diagnosis of Nephrotic Syndrome

Protein- loosing enteropathyHepatic failure

Protein energy malnutrition

Acute and chronic GN

Urticaria & Angioedema

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Relevant definitions

Remission:

Trace or negative on dipstick or proteinuria <4 mg/m²/h or urinary P/C ratio <200 mg/g (20 mg/

mmol

) for 3 consecutive days

Relapse

:

Urine albumin 3+ or 4+ or proteinuria >40 mg/m²/ h or urinary P/C ratio >200 mg/g (20 mg/

mmol

) for 3 consecutive days

Frequently relapsing:

≥2 relapses within 6 months of initial response or ≥4 in any 12 month period

Steroid-dependent

:

2 consecutive relapses occurring while weaning to alternate day steroids or within 2 weeks of steroid discontinuation

Steroid-resistant

:

Persistent proteinuria despite 60 mg/m² or 2 mg/kg for 8 weeks, after ensuring no infection or non-adherence to medication

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Natural Evolution of N. S.

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Pathology

Most children do not get a kidney biopsy MCD or FSGS

Minimal change, Normal glomeruli under LM, with podocyte effacement by EM

Characteristic histology in FSGS is segmental sclerosis of affected glomeruli, with the segment often adherent to Bowman’s capsule by

synechiae

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MCD

FSGS

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Second line investigations in NS

Complement C3, C4 Antinuclear antibody (ANA)

Anti-double- stranded DNA (anti-dsDNA) and ANCA

Hepatitis B and C (

HBsAg

, anti HCV)

Anti HIV antibodies

Genetic mutation analysis

Renal biopsy

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Indications for Renal biopsy At onset

Age 10yrs

Gross hematuria, persistent microscopic hematuria

Low C3

Sustained hypertension

Renal failure not attributable to hypovolemia

Suspected secondary cause of

Proteinuria despite 4 weeks of daily steroids

Before initiating treatment with tacrolimus

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Incidence

1∙15 to 16∙9 / 100 000 children Highest in south Asian compared to European as reported in UK, South Africa, and Canada

SRNS: 2∙1 to 27∙3% and varies by country of origin

African–American children are more to have biopsy-proven FSGS (42–72%) & highest proportion of progression to ESRD as compared to European Americans

In south Asian children, FSGS is reported less commonly and ranges from 15- 39%

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Nephrotic syndrome Pathogenesis

Immune-mediatedSystemic circulating factors (

eg

,

suPAR

)

Podocyte related factors (eg

, ANGPTL4)

Genetic variants

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Immune Mediated: dysregulation of T lymphocytes

Supportive evidence

Efficacy of immunosuppressive agents in NS

Spontaneous NS remission following infection with measles

Resolution of NS following chemotherapy for Hodgkin’s and other T-cell lymphomas

Lastly, development of NS after allergic reactions to various stings and poisons

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Systemic circulating factors

Serum from patients with FSGS induced proteinuria or increased permeability of glomeruli to albumin

There was also successful treatment of recurrent FSGS after kidney transplantation with immuno- adsorption

Maternal transmission of FSGS confirmed a circulating factor

There are numerous factors proposed including:

Heparanase

,

Haemopexin

, Angiopoietin-like 4 (ANGPTL4),

Cardiotrophin

-like cytokine-1 and, more recently,

Soluble

Urokinase

Plasminogen activator receptor (

suPAR

)

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Genetics

Genetic risk and SSNS A genetic locus on chromosome 6p

and single nucleotide polymorphisms in HLA-

DQA1

&

DQB1

were associated with SSNS using an exome Array

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Genetics and SRNS

Mutations in podocyte genes- NPHS1, NPHS2, LAMB2, or WT1 explain 69–85% of CNS & 50–66% infantile NS

After first year, the chance of identifying a genetic cause for SRNS decreases

25% in 1- 6 years

18% in 7 - 12 years

11% in 13–18 years

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Mutant proteins

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Complications of Nephrotic Syndrome

InfectionVenous thromboembolism

Acute kidney injury (AKI)

Dyslipidemias

Subclinical Hypothyroidism,

Vit

. D deficiency,

Growth failure

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Infections

Major complication in NSIt triggers RelapsesCauses

Loss of Ig in the urine and impaired synthesis

Impaired T lymphocytes function

Loss of Compliment

Edema

Corticosteroids and Immunosuppressive agents

Malnutrition

Common infections: URTI, peritonitis, Cellulitis,

othrs

Encapsulated ( Pneumococci, H. Influenza), Gram

Neg

, viral ( Chicken pox)

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Thrombosis

Cerebral sinus venous thrombosis, pulmonary embolism, and renal vein thrombosisVTE occurs in 3% of cases of NS during childhood

platelet aggregation

increased synthesis of

prothrombotic

factors (factors V and VIII)

urinary loss of

antithrombin

III, protein C and S

altered fibrinolysis

intra vascular fluid depletion

Treatment with low-molecular-weight heparin

There is insufficient evidence to warrant universal thrombosis prophylaxis in childhood NS

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Acute Kidney Injury in Nephrotic Syndrome

3rd most important complication in NS

58∙6% of 336 children admitted to hospital for NS

Diuretics in hemoconcentration

Intravascular volume depletion

Renal vein thrombosis

ATN in the setting of hypovolemia and sepsis

Interstitial nephritis induced by non-steroidal anti-inflammatory drugs or antibiotics

Intrarenal edema

Transformation of underlying glomerular disease (e.g., crescentic nephritis superimposed on membranous nephropathy)

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Dyslipidemia

The use of lipid lowering agents for the dyslipidaemia in NS is not advised, unless there is substantial persistent proteinuria with extremely high levels of hypertriglyceridaemia

If statins are initiated, it is only recommended for children over the age of 10 years with monitoring of liver function and creatinine kinase prior to initiating therapy and after 4 weeks

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Management Edema in nephrotic syndrome

Salt and fluid restriction with addition of a loop diuretic for severe or symptomatic edema Albumin infusion, in combination with a loop diuretic

Administration of albumin in children with signs of hypovolemia, as the resultant expansion in intravascular fluid could precipitate pulmonary edema

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Frequent relapsing -FRNS

Low-dose, alternate-day steroid , typically at the lowest dose possible, or just above the steroid dose associated with the latest relapse

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Several trials suggest that relapses might be reduced if prednisolone is administered daily for 5–7 days at the onset of upper respiratory tract infection in FRNS or SDNS

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Side Effect of Chronic Steroid Use

Obesity Cushingoid features Striae

Ocular complications, cataracts & glaucoma,

Metabolic features

Osteoporosis and avascular necrosis of the head of the femur

Behavioural

features

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Steroid Sparing agents

LevamisoleCyclophosphamideCalcineurin inhibitor: Cyclosporine and Tacrolimus

Mycophenolate mofitel

Rituximab

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Treatment for Steroid-Resistant Nephrotic Syndrome

Genetic testing Kidney biopsy

CNIs (

ciclosporin

& tacrolimus) are recommended as initial therapy for children with SRNS

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Immunization in Nephrotic syndrome

Live vaccines are contraindicated

if the child is on steroids

OPV should not be given to siblings of children with active nephrotic syndrome

Killed/adjuvant vaccines when in remission or on alternate day steroids of 0.5 mg/kg

Annual influenza vaccine

Varicella

2 doses at 3 months interval

Pneumococcal conjugate vaccine

Children 24 - 71 months who received 3 doses previously - administer 1 dose of PCV13

Received < 3 doses of PCV 13 - 2 doses of PCV13 (Both are followed by PCV 23)

6 to 18

yrs

, previously unvaccinated children- a single dose of PCV13 & PCV23 at 8 weeks apart

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ACUTE KIDNEY INJURY

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Sudden deterioration in renal function results in the inability of the kidneys to maintain fluid and electrolyte homeostasis.

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AKIN Classification

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Etiologies: a general approach

Though likely multifactorial, can be divided into:

Pre-renal

Renal

Post-renal

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Urinary Neutrophil Gelatinase-Associated Lipocalin (NGAL)

Urinary Interleukin 18Urinary Kidney Injury Molecule 1 (KIM-1)Cystatin C

New Biomarkers in AKI

Alternatives to Serum Creatinine

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Epidemiology of AKI

Incidence (US): 0.8/100 000≈ 7% of hospitalized patients.36 – 67% of critically ill patients (depending on the definition).5-6% of ICU patients with AKI require RRT.Mortality in

critically ill

pts with AKI requiring RRT 50-70%.

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Inhibition of tubular creatinine secretion

Trimethoprim, Cimetidine, ProbenecidIncrease in Creatinine without AKI

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Increased production GI Bleeding

Catabolic states (Prolonged ICU stay) Corticosteroids Protein loads (TPN-Albumin infusion)Increase in BUN without AKI

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Renal causes

Vascular:

Microvasculature:

Sickle cell disease

HUS

Tumour lysis

rhabdomyolysis

Glomerular:

Glomerulonephritis:

Post-infectious

membranoproliferative

SLE

HSP

Tubulo/Interstitial:

Acute tubular necrosis

-

secondary to nephrotoxic

insults or poor perfusion

Acute interstitial nephritis

-drugs

-infxn

Cortical dysplasia

-hypoxia/ischemia->infarct

-toxins/severe HUS

?

Sepsis

inflamm, not all volume related

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Acute TubularNecrosis

Describes an end effect of tubular damage… Secondary to perfusion insultsSecondary to toxinsChange in blood flow, obstruction and passive filtrate backflow into tubular cells can cause a cycle leading to further death…

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AIN

Drugs (71%) - 1/3 antibioticsPenicillins, cephalosporins, NSAIDs, sulfonamides, cipro, rifampin, PPIs, allopurinol… and moreInfection (15%)Strep, Legionella, leptospirosis, CMV, EBV… manyTubulointersitial nephritis and uveitis (5%)

Autoimmune

Idiopathic

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Nephrotoxins

Vascular effectACEi, cyclosporine, tacrolimusTubular effectProximal: aminoglycosides, amphotericin B, cisplatin, immunoglobulins, contrastDistal: NSAIDs, ACEi, lithium, cyclophosphamideObstruction: sulfa, acylovir, methotrexate AIN

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Post-renal causes

Two kidneys - distal or bilateral proximal obstructionSingle kidney - obstruction anywherePosterior urethral valves

Ureteropelvic junction obstruction

Ureterovesicular junction obstruction

Ureterocele

Stones

TumourHemorrhagic cystitisNeurogenic bladder

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Obtain a thorough history and physical.

Do everything you can to accurately assess volume status.Always order a renal ultrasound. Look at the urine.

Review urinary indices.

5 Key Steps in Evaluating AKI

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HISTORY

? pre-renal:Vomiting, diarrhea, bleeding, sepsis.Drug use - NSAIDs? renal:Bloody diarrhea? (HUS) Recent illness? (PSGN) Crush injury?

Drug use: aminoglycosides, antifungals, chemo

Associated lung/heart/liver symptoms? (dual organ)

? post-renal:

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Physical Examination

Pre-renal: DehydrationSigns of heart failure/cirrhosis/sepsisRenal:Edema (nephrotic syndrome)

Purpura (HSP)

Post-renal: palpable bladder?

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What to order?

BUN, Cr, lytes, fractional excretion of sodiumUrinalysis

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Normal Cr varies by age

Age

Normal range (mg/dl)

Newborn

0.3 to 1

Infant

0.2 to 0.4

Child

0.3 to 0.7

Adolescent

0.5 to 1

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Urinalysis

NORMAL:-pre-renal (may be concentrated)-post-renal

-ATN

ABNORMAL:

-brown granular/epithelial

casts = ATN

-red cell casts =

Glomerulonephritis

-pyuria, white cell casts = UTI

or glomerulonephritis (post-

infxn)

-

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Urine osmolality:

Typically low in ATN (<350 mosmol/kg)Typically high in pre-renal disease (>500)Urine volume: Often low, especially given criteria for AKI.

However, some ATN is non-oliguric

Urine eosinophils

Urine sodium…

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Sodium excretion

Why? Helps distinguish pre-renal vs ATN…>30-40 mEq/L = ATN<10 mEq/L = effective volume depletion(20-30 in infants)BUT what if there is a large urine output?

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Fractional Excretion of Sodium

FENa compensates for the urine output…UNa x PCr PNa x UCr…can also be thought of asUNa/PNa

UCr/PCr

<1% --> pre-renal disease

1-2% --> ??

>2% --> ATN

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Bloodwork…

CBC: look for MAHA, thrombocytopenia Extended lytes. Renal injury can result in:HyperkalemiaHyperphosphatemia HypocalcemiaMetabolic acidosisOther options, depending on history: ANCA,

ANA, ASOT, complement, drug levels…

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Imaging

Ultrasound - in all children if etiology unclear# of kidneysSize of kidneysObvious parenchymal damageObstruction Thrombus/vessel occlusion

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Renal biopsy

Only when diagnosis remains unknown, or there is a failure to respond to treatment

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RRT

Options:Continuous renal replacement therapyPeritoneal dialysisHemodialysis

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Prognosis

Mortality: 60% (critically ill) 20-25% go on to have some degree of chronic renal issues

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Creatinine

None sensitive, > 50% of kidney function to be lostVaries with age, muscle mass, gender Tubular secretion

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TREATMENT - Medical Management

Obstruction- PUV: bladder cath should be placed immediately for drainage volume status : If there is no volume overload or cardiac failure, isotonic saline, 20 mL/kg over 30 min.

After volume resuscitation, hypovolemic patients generally void within 2

hr

; failure to do so suggests intrinsic or

postrenal

AKI.

Hypotension caused by sepsis: vigorous fluid resuscitation followed by norepinephrine infusion

Furosemide (2-4 mg/kg) and mannitol (0.5 g/kg) may be administered as a single IV dose

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Hyperkalemia

> 6Stop Exogenous sources of potassium (dietary, intravenous fluids, total parenteral nutrition)Sodium polystyrene

sulfonate

resin (

Kayexalate

), 1 g/kg, should be given orally or by retention enema.

More severe elevations in serum potassium (>7 mEq/L), ECG changes • Calcium gluconate 10% solution, 1.0 mL/kg IV, over 3-5 min

• Sodium bicarbonate, 1-2

mEq

/kg IV, over 5-10 min

• Regular insulin, 0.1 units/kg, with glucose 50% solution, 1

mL

/kg, over 1 hr

β-adrenergic agonists

Persistent

hyperkalemia should be managed by dialysis.

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Metabolic Acidosis

< 7.15 to 12IV then oralCorrection of metabolic acidosis with intravenous bicarbonate can precipitate tetany

in patients with renal failure as rapid correction of acidosis reduces the ionized calcium concentration

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Management of ↑PO4 and ↓Ca

Hyperphosphatemia:Low phosphate dietBindersHypocalcemia:Calcium gluconate if Tetany.Usually by ↓ PO4

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Others

Hypertension AnemiaGI protectionNeurological disorders

Dialysis

Nutritional support

Slide115

Indication of Dialysis

• Anuria/oliguria

• Volume overload with evidence of hypertension and/or pulmonary

edema refractory to diuretic therapy

• Persistent

hyperkalemia

• Severe metabolic acidosis unresponsive to medical management

• Uremia (encephalopathy,

pericarditis

, neuropathy)

• Blood urea nitrogen >100-150 mg/

dL

(or lower if rapidly rising)

•

Calcium:phosphorus

imbalance, with hypocalcemic

tetany

that

cannot be controlled by other measures

Slide116

Questions