6 th Year Medical school Dr Reham Almardini Outline Introduction Hematuria Proteinuria Tubulopathy HUS Acute Kidney Injury CKD RRT Urology UTI Introduction Retroperitoneal space ID: 909910
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Slide1
PEDIATRIC NEPHOLOGY MODULE
6th YearMedical school
Dr.
Reham
Almardini
Slide2Outline
Introduction HematuriaProteinuriaTubulopathy
HUS
Acute Kidney Injury
CKD
RRT
Urology- UTI
Slide3Introduction
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
Slide4Nephrons 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
Slide5Functions of the kidneys
Filtration and excretion of fluid &waste products Bp. controlAcid base balance Production of Erythropoietin and renin
Activation of vitamin D
Slide6Hematuria
Slide7Definitions 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
Slide8False positive: Hemoglobin, myoglobin, oxidizing agent as hypochlorite, UTI- microbial peroxidases
False negative; reducing substances as Ascorbic acids, high specific gravity
Slide9Slide10Hemoglobinuria # Myoglobinuria
Cola colored urine
Slide11Rhabdomyolysis
Slide12Incidence 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
Slide13Slide14Slide15Causes 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)
Slide16Gross 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
Slide17Causes of recurrent gross hematuria
IgA nephropathyFamilial benign hematuriaAlport Syndrome
Nutcracker syndrome
Slide18In 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
Slide19Features 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
Slide20Glomerular
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
Slide21Glomerular 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
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
Slide23Alport’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
Slide24History
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
Slide25Slide26Slide27Slide28Investigation
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
Slide29Investigation
Slide30If the microscopic hematuria persists unchanged for more than 1–2 years further evaluation is recommended
Slide31Indication 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
Slide32Questions
Slide33Hemolytic-Uremic
Syndrom
Slide34Hemolytic-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
Slide35Hemolytic-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
Slide36Prognosis 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
Slide37Treatment
D+ HUS: SupportivePneumoccocal; Prompt disease treatement
, washed RBC
Plasma therapy in genetic , ADAMST13
Eculizumab
Slide38Idiopathic 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
Slide39Hypercalciuria
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
Slide40Proteinuria
Slide41Children: 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
Slide42False Positive Dipstick
Very Alkaline Urine- some UTIHematuria
Very concentrated urine( SG> 1.030)
Chlorohexidine
Contamination
Slide43Causes of proteinuria
Non Pathological causesOrthostatic
Febrile
Exercise induced
Pathological Causes
Tubular (Allergic interstitial nephritis, ATN)
Glomerular ( NS, GN)
Slide44Nephrotic Syndrome
Slide45Clinical 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)
Slide46Slide47Differential Diagnosis of Nephrotic Syndrome
Protein- loosing enteropathyHepatic failure
Protein energy malnutrition
Acute and chronic GN
Urticaria & Angioedema
Slide48Relevant 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
Slide49Natural Evolution of N. S.
Slide50Slide51Pathology
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
Slide52MCD
FSGS
Slide53Second 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
Slide54Indications 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
Slide55Incidence
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%
Slide56Nephrotic syndrome Pathogenesis
Immune-mediatedSystemic circulating factors (
eg
,
suPAR
)
Podocyte related factors (eg
, ANGPTL4)
Genetic variants
Slide57Immune 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
Slide58Systemic 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
)
Slide59Genetics
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
Slide60Genetics 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
Slide61Mutant proteins
Slide62Complications of Nephrotic Syndrome
InfectionVenous thromboembolism
Acute kidney injury (AKI)
Dyslipidemias
Subclinical Hypothyroidism,
Vit
. D deficiency,
Growth failure
Slide63Infections
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)
Slide64Thrombosis
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
Slide65Acute 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)
Slide66Dyslipidemia
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
Slide67Slide68Management 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
Slide69Slide70Frequent relapsing -FRNS
Low-dose, alternate-day steroid , typically at the lowest dose possible, or just above the steroid dose associated with the latest relapse
Slide71Several 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
Slide72Side 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
Slide73Steroid Sparing agents
LevamisoleCyclophosphamideCalcineurin inhibitor: Cyclosporine and Tacrolimus
Mycophenolate mofitel
Rituximab
Slide74Treatment for Steroid-Resistant Nephrotic Syndrome
Genetic testing Kidney biopsy
CNIs (
ciclosporin
& tacrolimus) are recommended as initial therapy for children with SRNS
Slide75Slide76Immunization 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
Slide77ACUTE KIDNEY INJURY
Slide78Sudden deterioration in renal function results in the inability of the kidneys to maintain fluid and electrolyte homeostasis.
Slide79Slide80Slide81AKIN Classification
Slide82Etiologies: a general approach
Though likely multifactorial, can be divided into:
Pre-renal
Renal
Post-renal
Slide83Slide84Urinary Neutrophil Gelatinase-Associated Lipocalin (NGAL)
Urinary Interleukin 18Urinary Kidney Injury Molecule 1 (KIM-1)Cystatin C
New Biomarkers in AKI
Alternatives to Serum Creatinine
Slide85Epidemiology 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%.
Slide86Inhibition of tubular creatinine secretion
Trimethoprim, Cimetidine, ProbenecidIncrease in Creatinine without AKI
Slide87Increased production GI Bleeding
Catabolic states (Prolonged ICU stay) Corticosteroids Protein loads (TPN-Albumin infusion)Increase in BUN without AKI
Slide88Renal 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
Slide89Acute 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…
Slide90AIN
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
Slide91Nephrotoxins
Vascular effectACEi, cyclosporine, tacrolimusTubular effectProximal: aminoglycosides, amphotericin B, cisplatin, immunoglobulins, contrastDistal: NSAIDs, ACEi, lithium, cyclophosphamideObstruction: sulfa, acylovir, methotrexate AIN
Slide92Post-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
Slide93Obtain 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
Slide94HISTORY
? 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:
Slide95Physical Examination
Pre-renal: DehydrationSigns of heart failure/cirrhosis/sepsisRenal:Edema (nephrotic syndrome)
Purpura (HSP)
Post-renal: palpable bladder?
Slide96What to order?
BUN, Cr, lytes, fractional excretion of sodiumUrinalysis
Slide97Normal 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
Slide98Urinalysis
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)
-
Slide99Urine 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…
Slide100Sodium 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?
Slide101Fractional 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
Slide102Bloodwork…
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…
Slide103Imaging
Ultrasound - in all children if etiology unclear# of kidneysSize of kidneysObvious parenchymal damageObstruction Thrombus/vessel occlusion
Slide104Renal biopsy
Only when diagnosis remains unknown, or there is a failure to respond to treatment
Slide105RRT
Options:Continuous renal replacement therapyPeritoneal dialysisHemodialysis
Slide106Prognosis
Mortality: 60% (critically ill) 20-25% go on to have some degree of chronic renal issues
Slide107Slide108Slide109Creatinine
None sensitive, > 50% of kidney function to be lostVaries with age, muscle mass, gender Tubular secretion
Slide110TREATMENT - 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
Slide111Hyperkalemia
> 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.
Slide112Metabolic 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
Slide113Management of ↑PO4 and ↓Ca
Hyperphosphatemia:Low phosphate dietBindersHypocalcemia:Calcium gluconate if Tetany.Usually by ↓ PO4
Slide114Others
Hypertension AnemiaGI protectionNeurological disorders
Dialysis
Nutritional support
Slide115Indication 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
Slide116Questions