Jam, Richelle, April, Anne Page 1 of 7
IV.1 – Nephrology
Dr. Doctor
December 9, 2013
*Normal text = Doc’s powerpoint*Italicized text = Notes from lecture
*Text inside dashed boxes = Notes from last year’s trans/ Nelson
KIDNEY AND URINARY TRACT
I. KIDNEYS Nephron Glomerulus Tubules - Calyces Interstitium Special Cells II. URETER
III. URINARY BLADDER
Urinary Bladder Junction Urethral Valve/ Sphincter
Figure 1. Pediatric Urinary Tract
Table 1. Organs of theUrinary Tract and their Functions
PART FUNCTION
Kidneys A pair of organs that filter the blood of the waste, unused minerals, and water that make up urine.
Calyx Small chambers in the kidneys that drain urine into the renal pelvis
Renal Pelvis Where urine collects before flowing down the ureters
Ureters A pair of tubes that carry urine from the kidneys to the bladder
Bladder An organ that stores urine until the child is ready to release it.
Ureterovesical
junction Valve function which is responsible for protection of the low pressure upper urinary tract from the refluxing of urine from the bladder
Sphincters Ring-shaped bands of muscles. The urethral sphincters work together to hold in or release urine from the bladder. They close and tighten to hold and open and relax to release.
Nerves Signal when the bladder is filled with urine. They also tell the sphincter and bladder when it’s time to empty the bladder.
Urethra Tube that carries urine from the bladder out of the body
KIDNEYS OF A NEWBORN INFANT
Relatively large and can usually be palpated through the anterior abdominal wall
Mean combined weight of both kidneys at birth 6 months = 24 g
12 month = 70 g 6 years old = 140 g Adult weight = 300 g
NEPHRON
Structural and functional unit of the renal parenchyma At 36th week of gestation, nephrogenesis stops and
each kidney has 850,000 to 1M nephrons
Each nephron consists of glomerulus and its tubules For urine formation, acid-base balance, secretion of
certain substances
Each glomerulus is made of capillary tufts enclosed in Bowman’s capsule
Capillary tufts consists of loops bound together in a central area called mesangium
Mesangium is composed of cytoplasmic matrix and cells (mesangial or capillary); it is usually the first to react in the event of glomerular insult
3 fixed cells of glomerulus: Endothelial or intracapillary cell Mesangial cell
Epithelial or extracapillary cell
3 PRICINCIPLES OF KIDNEY FUNCTION
1. Maintain constancy of internal environment by adjusting volume, concentration and composition of body fluids
2. Elimination of metabolic wastes such as urea and creatinine
3. Elaborate the hormones renin, erythropoietin, prostaglandin kallikrein-kinin
URINE FORMATION
Initiated by elaboration of a large volume of protein-free plasma ultrainfiltrate through glomerular filtration Concentration and alteration of filtrate composition in
the tubules (through tubular reabsorption of essential substances and elimination of waste products)
PROXIMAL TUBULES
Reabsorbs 80% of filtrate volume and sodium All the glucose and amino acids (small portion) and
much of the filtered phosphate
Primary active process is Na+ reabsorption
Followed by passive reabsorption of Cl- and H2O by diffusion
Volume is greatly reduced but Na+ and Cl- not altered
LOOP OF HENLE
Water is reabsorbed in the descending limb Na+ is reabsorbed in the ascending limb
Result is an environment in the interstitial tissue of medulla that is hypertonic to plasma thus urine concentration takes place in the adjacent collecting ducts
Fluid at the end of the loop is hypertonic
DISTAL TUBULES
Fluid is initially hypotonic to plasma due to large amount of Na+ reabsorbed in the ascending limb More Na+ reabsorbed due to aldosterone
K+ is secreted
COLLECTING DUCT
Final concentration mediated by vasopressin acting on the lining cells of the duct making them more
permeable to water
Table 2. Glomerulus and Tubules
GLOMERULUS TUBULES
BP, Volume Concentration If decreased filtration
→decreased blood flow →decreased output→ decreased urine volume
Responsible for increased urine concentration Overcrowding/ inflammation →oliguria/anuria Tubulo-interstitial nephritis Additional notes:
Normal Kidney – 1M nephrons Mechanism of Urination:
Gravitational pull of the fluid →Detrusor muscle distention →Sphincter opening
Normal GFR
Adult: 100-120 mL/min or approximately 2L filtration/day
1% goes down as urine (700-1500 mL/day) Excreted metabolic acids – 1 mEq/kg In children: Ureters are dilated
DIAGNOSTIC MODALITIES URINALYSIS Physical Color Turbidity Specific gravity Acidic/ Basic Odor Microscopic
Red Blood Cells (RBC) White Blood Cells (WBC) Crystals Other Cells Casts Chemical Sugar Protein Pigments – e.g.Bilirubin Electrolytes – Na, K, Cl, Ca, Mg
Ketones – appears when you have starvation Uric acid – will predispose to crystal formation Urea – due to high protein intake
ANATOMIC IMAGING Gross
Ultrasound
o KUB with Prevoid-Postvoid image X-ray
a. Plain b.Contrast
o Intravenous Pyelogram (IVP) – an x-ray picture of the kidneys and ureters after injection of a radiopaque dye; used to locate kidney stones and to determine the anatomy of the kidney
o Voiding Cysto-urethrogram (VCUG) - a minimally invasive test that uses a special x-ray technology called fluoroscopy to evaluate a child's bladder size, shape, and capacity, as well as the urethra. This procedure can also determine if a child has reflux — a condition where urine from the bladder goes upward back to the kidneys. This exam may be ordered after a child experiences frequent urinary tract infections.
Vascular Imaging o Angiogram o Echoangiogram Scan o Technetium Scan o CT-Scan –anatomic
o Magnetic Resonance Imaging (MRI) – vascular and anatomic
BLOOD TESTS
Complete Blood Count, Hemoglobin, Hematocrit,
WBC, RBC, platelets, Bilirubin Chemical
Blood Urea Nitrogen (BUN), Creatinine Electrolytes
Protein, sugar
Hemolytic products –to diagnose Hemolytic Uremic Syndrome
Immunologic Products - e.g.to diagnose IgA nephropathy,
Systemic markers – Anti-neutrophil cytoplasmic antibody (ANCA), Anti-neutrophilic antibodies (ANA); useful for diagnosis of glomerulonephritis
HISTOLOGY Light Microscopy
Electron Microscopy
Micropuncture Functional Studies
CLINICAL DISEASES IN CHILDREN
URINARY TRACT INFECTION Urethra and Bladder
Ascending peri-anal and intestinal bacteria – no. 1 cause is E. coli
Fungal
Common age group: 3 y/o and below. (Can be Up to 5 y/o)
In girls, the first UTI usually occurs by the age of 5 yr, with peaksduring infancy and toilet training
In boys, most UTIs occur during the 1st yr of life UTIs are caused mainly by colonic bacteria
In girls, 75-90% of all infections are caused by Escherichia coli,followed byKlebsiellaspp and Proteus spp
Usually manifests as Proteinuria + Pus in urine Upon urination → bacteria will stick to urethra →
migrateupwards → causing CYSTITIS (inflammation of bladder wall) →when bladder contracts, there is pain→ irritable muscles, nerveendings → epithelium is affected →dysuria
Cystitis indicates that there is bladder involvement. Symptoms include dysuria, urgency, frequency,
suprapubicpain, incontinence, and malodorous urine. Cystitis does not cause fever and does not result in
renal injury
Recurrent UTI- common cause of Rena Failure
During infancy, valve effect of ureterovesical junction is still very weakpredisposing them to vesicoureteral reflux
When there is predominant WBCs and proteinuria in urinalyis, plus fever → it is best to presume that this
ispyelonephritis rather than just simple lower UTI→aggressive treatment needed to protect kidneys
and prevent renal insufficiency. The 3 basic forms of UTI:
Pyelonephritis Cystitis
Asymptomatic bacteriuria
SIGNS AND SYMPTOMS OF UTI A. LOWER URINARY TRACT INFECTION Dysuria
Frequency/ small amounts Non-specific discomfort
Fever is infrequent (but may be positive)
B. UPPER URINARY TRACT INFECTION/PYELONEPHRITIS
Fever and systemic signs – patient becomes highly febrile because toxins and antigens go to the highly vascular kidneys; pag highly febrile ang patient, usually Upper Urinary Tract ang involved; High fever also denotes a more serious infection
Flank pain
Non-specific signs of serious illness
DIAGNOSIS A. DIRECT (localized)
Urinalysis
Shows Increased WBC (>5/hpf) +/- RBCs
Pyuria (leukocytes in urine) suggests infection, but infection can occur in the absence of ofpyuria; this finding is more confirmatory than diagnostic. Conversely, pyuria can be present without UTI. Urine Culture/Sensitivity
Usually reveals E. coli
Usually 100,000 (105) CFU but may also be 104 or 103because frequent urination may provide less time for bacteria to grow, thus less bacteria are detected in Urine C/S
Child who is sick with 100,000 colonies definitely UTI but should present with pus cells in urinalysis
o 10,000 colonies + symptoms diagnose as UTI o 1,000 colonies + symptoms diagnose as UTI
B. SYSTEMIC
CBC – Increased WBC, Anemia in chronic disease Blood C/S
Creatinine – measures excretion function In children: Normal Creatinine = 0.4-0.8
mg/dL
In adults: Normal Creatinine = 1-1.5 mg/dL
C. ANATOMIC IMAGING
Ultrasound – more useful for Upper UTI Bladder – thickened, irregular
Ureters – visible, wide and with abnormal contour Kidneys – enlarged in UTI, small in chronic cases
due to scar formation wherein dead nephrons are replaced by non-functional scar tissues
X-ray – allows visualization of stones Technetium
To visualize scars
Shows delayed opacification Shows delayed excretion
Shows contracted or enlarged kidneys
TREATMENT Empiric
Ampicillin
Co-amoxiclav + Aminoglycoside
Parenteral antibiotics – expect improvement after 3 days. If urinalysis appears to be normal already, patient may shift to oral antibiotics to complete the recommended 7-day regimen.
Based on Culture and Sensitivity Results –takes 48 to 72 hours, so empiric treatment may be given first. If the patient shows to be sensitive to the empiric
treatment given and has a good response then the antibiotic may be continued. If (-) sensitivity but (+) good responses, it’s up to the physician to decide whether to change the antibiotic or not.
Follow-up Treatment
Urinalysis – to see if the urine has improved or if the patient is responding well to treatment
Culture and Sensitivity - sometimes done to know if there is still some bacteria left
Follow-up imaging – changes in the kidney may be seen after 6 months to 1 year. e.g. scar
formation will not become normal until 6 months to 1 year
VESICO-URETERAL REFLUX NORMAL URINARY TRACT
Vesicoureteric junction does not allow retrograde flow of urine from bladder to the kidney
VESICOURETERAL REFLEX
Phenomenon of backward-upward flow of urine Permit transport of urine from bladder to the kidney May be uni-/bilateral
Demonstrated and grade by Voiding Cystourethrogram
PATHOPHYSIOLOGY
Bacterial invasion and multiplication →Inflammation and host reaction →Loss of normal renal function →Necrosis of renal tissue
Aggressive treatment is done to avoid destruction of the area
1. BACTERIAL INVASION AND MULTIPLICATION Bacteria from stools
Proximity of urethra
Adherence of E. coli that resists urine flow
Ascends from urethra to bladder (cystitis, lower UTI) Ascends from bladder to ureters (reflux)
Ascends from ureters to kidney (pyelonephritis) Low to negative bacterial growth by culture and
sensitivity
Short bladder time = newborn and infants Low dose antibiotics
Wrong culture and media used
2. INFLAMMATION AND HOST REACTION Bladder irritation
o Hypercontracted bladder wall →frequent small amount of urine
To diagnose bladder function, UTZ shows bladder walls thicker than normal
Inflammation →edema→thickening of walls Increased WBC during inflammation Diluted urine due to failure to concentrate Glomerulus is not affected so filtration is not
affected
Creatinine clearance – for kidney function test Kinds:
a. Urethritis
o Dysuria, burning sensation b. Cystitis
o Dysuria, bladder tenderness, frequent urination with fever
o On UTZ: thickened bladder wall c. Pyelonephritis
o Systemic symptoms 3. LOSS OF RENAL FUNCTION
Decreased number of nephrons Nephron hypertrophy →early aging
→hyperfiltration→nephrosclerosis→destruction (proteinuria and HTN) →renal insufficiency →renal failure
4. NECROSIS OF RENAL PARENCHYMA
Tubule and surrounding intersitium are inflamed Destruction of growth of functional cells (growth
factors, vit D, erythropoietin, prostaglandins, hormones)
Tubule destroyed, glomerulus obliterates Area replaced by non-functional scar tissue Number of nephrons are reduced
REFLUX GRADING
Figure 2. Reflux grading (Nelson) Table 3.Reflux Grading
GRADE DESCRIPTION
Grade 1 Reflux into a nondilated ureter
Grade 2 Reflux into the upper collecting system without dilation
Grade 3 Reflux into a dilated ureter and/or blunting of calycealfornices
Grade 4 Reflux into a grossly dilated ureter
Grade 5 Massive Reflux with significant dilatation and tortuosity and loss of capillary impression
WHAT TO DO WITH PYELONEPHRITIS: VESICOURETERAL REFLUX
1. Prophylactic Antibiotic – continuous prophylactic low dose single daily antibiotic. Advise to take nightly so in the morning, the patient will urinate. So there is a long period of time for antibiotics to stay in the body. However, this is only effective in older children and adults because infants urinate every 2 hours. Ditopapasokyungsinabini doc na choice of antibiotic. It may either be
a. 500 mg penicillin – it is very effective but after 4 hours it will already be excreted leaving the urinary tract vulnerable for infection again b. Cotrimoxazole – after 12 hours (6 to 8 hours sa
past trans), drug will concentrate in the kidneys. If the patient sleeps (without urinating) and urine refluxes, he/she is protected because the antibiotic is still present. Cotrimoxazole is the one used in adults or older children
2. Reflux repair by re-implantation of ureter by urologist 3. Periodic urinalysis/ Culture and sensitivity to
document recurrent UTI – must be done especially
if patient experiences recurrent UTI as this poses a higher risk for vesico-ureteral refulx
4. Health status monitoring a. Renal function
b. Anthropometric evaluation 5. Follow-up imaging
a. For anatomic changes – scar formation b. For determination of functional status 6. Blood tests for evaluation of renal function
POST-INFECTIOUS ACUTE
GLOMERULONEPHRITIS/ POST-STREPTOCOCCAL ACUTE GLOMERULONEPHRITIS (PSAGN) The usual age group affected: 4-9 years old
Accdg to Nelsons, PSGN most common in children aged 5-12 yr and uncommon before the age of 3 yr.
4 features of AGN Edema
Oliguria HPN Hematuria
Depending on the severity of renal involvement, patients can develop various degrees of edema, hypertension, and oliguria.
Nonspecific symptoms such as malaise, lethargy, abdominal pain, or flank pain are common.
AGN is not an infection but an immunologic disease depression in the serum complement (C3) level
provide strong evidence that ASPGN is mediated by
immune complexes
Occurs AFTER strep infection→ PSAGN Group A β-hemolytic streptococcal
(GABHS)infections are common in children and can
lead to the postinfectious complication of acute glomerulonephritis (GN)
The usual infection is not sore throat.
In rheumatic fever, it is usually sore throat.
In PSGN, it is usually streptococcal skin infection. The typical patient develops an acute nephritic
syndrome 1-2 wk after an antecedent streptococcal pharyngitis or 3-6 wk after a streptococcal
pyoderma
The history of a specific infection may be absent, because symptoms may have been mild or have resolved without patients receiving specific
treatment or seeking the care of a medical provider. There is predominantly RBC in PSGN
Also presents with proteinuria, but this isn’t used as a criterion.
Sometimes will have small amount of WBC because it is an inflammatory disease, but more predominant ang RBC (10-15 WBC, 20 RBC)
Presence of signs of inflammation: edema, swelling,
dysfunction
In PSGN: edema of capillaries spaces becomes small filtration and excretion of water and solutes become impaired→edema, HPN, oliguria, hematuria.
Fluid retention→edema
o Starts perioorbitally, noticeable upon waking up o Gravitates towards lower extremities on
prolonged standing o Taut but puts on pressure Unable to excrete fluids →oliguria
o Voids rarely or goes to toilet frequently without passing out urine
Fluid overload→ congestion
Will produce some escape of RBC’s →hematuria o Varies from microscopic to gross
o Frankly bloody, smoky brown or tea-colored o Most alarming sign but not an indication for
admission
Fluid overload and congestion →hypertension o Nuchal pain, headache, vomiting, transient
visual loss
o Systolic and diastolic BP levels are generally above 120/80 mmHg, respectively
o Patients are at risk for developing encephalopathy and/or heart failure secondary to hypertension or hypervolemia.
o Hypertensive encephalopathy must be considered in patients with blurred vision, severe headaches, altered mental status, or new seizures
Hematuria is not an indication for admission. Usually they are admitted due to edema or congestion or problematic blood pressure
Table 4. Comparison between UTI and PSAGN
UTI PSAGN
Increased WBC shown in
urinalysis Increased RBC Usually involves tubules,
interstitium Involves the glomerulus + Protein + Protein, small
amounts
Sepsis and Scar Good recovery in 6 to 8 weeks
Normal volume of urine
Figure 3.Clinical Course of PSAGN
Typical course lasts for 7 to 10 days for each of the three phases:
1.Oliguric Phase
o Acute salt and water overload
o Complications: hypertensive encephalopathy, renal failure, CHF
o Phase shortened by the use of parenteral diuretics
2.Diuretic Phase (3-5 days)
o Levelling of the daily weight curve, then spontaneous voiding or sudden volume increments with diuretic agents
o BP normalizes and the child starts feeling better 3.Immediate Convalescent
o Most hospitalized children are ready for discharge o All alarming indices in the oliguric period are gone
except for residual gross or significant microscopic hematuria.
DIAGNOSIS/FEATURES OF GLOMERULAR DISEASES
A. Urinalysis
Gross (macroscopic) hematuria Normal to high specific gravity Mild to absent WBC
RBC casts ± protein
B. Blood tests
CBC = normal or with slight anemia Serum protein (albumin) = normal
BUN, Creatinine = Normal or <10% azotemia ± electrolytes
C3 = low
C. Imaging
Normal to enlarged kidney
Screen to rule out systemic disease like SLE or HSP Acute Glomerulonephritis should subsidein 8 weeks
to 1 year
o If it recurs after 8 weeks, it is now considered as chronic renal disease or chronic
glomerulonephritis
o No recurrence after 6 months to 1 year means good prognosis
D. Biopsy
1-5% progress to RPGN
Recurrence of signs and symptoms implies non-post infection streptococcal AGN
Biopsy indicated if signs and symptoms persist
with atypical presentation
Not indicated with improvement of signs and symptoms
Remember that PSAGN usually does not recur
E. Anti-streptolysin O titer (ASO titer)
usually negative
F. Anti-DNAse titer
Positive in post-skin infection but not during the infection
TREATMENT
Hematuria is not an indication for hospital admission; no treatment for this; furthermore, anemia from hematuria is INSIGNIFICANT
Oliguria and edema are indications for admission as they may lead to complications such as CHF, hypertensive encephalopathy, etc.
Water and salt restriction. Limit to 3 mg/kg/day Sodium intake
Diuretics like Furosemide
Hypertension is due to water restriction Water and salt restriction
Antihypertensives/diuretics like Furosemide
Post-streptococcal infection
May be treated with Penicillin – to eliminate any residual carrier state for Streptococcus which may be infect other people
NEPHROTIC SYNDROME (MINIMAL CHANGE DISEASE)
Age incidence: 1-3 yrs old onset
Minimal change glomerular histopathologic disease (or no change that can be seen by light microscopy) Electron microscopy
Basement membrane immune deposits Selective albuminuria (proteinuria) – passage of
albumin to the basement membrane
Massive albuminuria greater than 1 g/m2/24 hours (>40mg/m2/hour)
Edema
Massive proteinuria Hypoalbuminemia
Hyperlipidemia – usually present, but not necessary to diagnose the disease because if you already have massive proteinuria, then it is already diagnosed as NS
Hypotension
Postural hypotension (orthostatic) No hematuria, no pyuria
In nephrotic syndrome, the presentation are edema which may have normal BP or hypotension (unlike glomerulonephritis which has hypertension as
manifestation)
Nephrotic syndrome is not just proteinuria, it is
massive proteinuria compared to other proteinuric
states of other disease
There is also hypovolemia in NS due to loss of albumin in the urine
90% of NS that presents with edema, massive proteinuria and hypoalbuminemia – typically will have
hematuria
Usually associated with hypocalcemia because calcium are mostly albumin-bound, thus when you lose albumin, you also lose calcium
DIAGNOSTIC TESTS
Urinalysis
+3 to +4 proteinuria
No or transient mild hematuria/pyuria(but not part of diagnostic criteria) No evidence of infection Hematuria Oliguria Edema Hypertension Gross to microscopic hematuria (minus edema and hypertension Microscopic hematuria Variants: 1. Chronic glomerulonephritis 2. Rapidly progressive glomerulonephritis (RPGN) Acute Stage = 7-14 days Diuretic Stage Recovery or Convalescent Stage Complete Recovery: 8 weeks average (6 mos to 1 year)
Systemic
CBC – normal (sometimes elevated platelet count) BUN, Creatinine – normal
C3 – normal Hyperlipidemia
Hypoalbuminemialess than 25 g/dl Hypercoagulability(prone to thrombosis)
o Blood volume is decreased, concentrated blood products.
o Aside from albumin, glomeruli are also excreting the blood products of anticoagulation thus the hypercoagulability
o Thus, you see to it that the blood extractions in these patients are atraumatic to prevent thrombosis
Anatomic Imaging – normal
Biopsy is not usually required but is indicated if there is:
Steroid resistance
Initial response followed by 2x resistance
Late age onset (12 years old and higher) – usually steroid resistance
TREATMENT
Prednisone
60 mg/m2/day – 4-6 weeks (divided into 3 doses;
after meal)
o You do not have to taper the dose until the 4th-6th week to prevent relapse of proteinuria
Taper the dose to 40 mg/m2/day(single dose in the morning) – you give this every other day for another 4-8 weeks
Prophylactic anti-TB (Isoniazid) – in the
Philippines, you do this because of the endemicity of TB in the country
When the patient becomes negative and no edema, the recurrence is usually induced by infections, usually upper respiratory tract infections in childhood
o In case of recurrence, you treat the infection, and resume Prednisone 60 mg/m2/day. You
may do it shorter or 4-6 weeks as long as the proteinuria has been negative for 3-5 consecutive weeks.
Good prognosis in 1-3 years old – good response
with steroids
Good prognosis if it is the classical presentation of NS DO NOT TREAT THE EDEMA OF NS WITH
DIURETICS – dangerous, worsens hypovolemia
May cause acute renal injury or significant oliguria because you are depleting further the blood volume
OTHER VARIETIES OF NS
Focal segmental glomerulosclerosis (FSGS) – IgA Nephropathy
Membranous glomerulonephritis
Progressive nephritis of systemic immunological disease (eg.SLE, HSP)
PROGRESSIVE RENAL DISEASE
Characterized by continuous deterioration of renal
function
Reduction of nephrons
Reduction of renal tissue (scarring) replacement by non-functional scars
Progression to azotemia
Anemia – associated with decrease in erythropoietin Growth and functional impairment
Uremic disease Renal failure
Electrolyte abnormalities No renal regeneration
Metabolic acidosis/alkalosis – but usually acidosis
ACUTE RENAL FAILURE (AKI/ARF)
Azotemia and oliguria – usual manifestation of ARF But there is also non-oliguric ARF but with azotemia Inflammation of glomerulus proliferation of
mesangial cells decrease filtration due to overcrowding of mesangial cells oliguria
Excretion of metabolic products azotemia Cardiovascular causes:
Hypovolemic dehydration Acute cardiac failure Vascular disease
o Large to small vascular diseases o Microvasculitis
Systemic Lupus Erythematosus (SLE) Kawasaki
HenochSchonleinPurpura (HSP) Triad: purpura, abdominal pain, renal
insufficiency
Also has arthritis or joint pain Hemolytic Uremic Syndrome (HUS)
Mild to moderate diarrhea Anemia
Oliguria Acidosis Convulsion
Due to infection like e. coli
Toxins will cause vasoconstriction of renal vasculature clumping of platelets and turbulence of flow hemolysis
Renovascular thrombosis (Renal Vein Thrombosis) Sepsis
Prematurity Toxins
Renal tubular injuries
o Example: Tumor lysis – causes hyperuricemia or increase uric acid which is toxic to the tubular epithelium
o Massive injury like crush syndrome – muscular destruction myoglobinuria (myoglobin is toxic to tubular epithelium)
o Some drugs
THERAPEUTIC CONSIDERATIONS
Associated symptoms with the antecedent cause May improve with withdrawal of the cause Need for supportive treatment
Rehydration (1st 72 hours) Nutrition
Electrolyte correction
Correction of acidosis/alkalosis Renal replacement therapy
Dialysis
In children, it is not easy to do hemodialysis, thus
peritoneal dialysis is preferred
RENAL TUBULAR DISEASES
Renal Tubular Acidosis – acidosis
Means tubules are losing a lot of bicarbonates Bartter’s Syndrome and Gittlman’s Syndrome –
alkalosis
A lot of acids are lost
Associated with failure to thrive, dehydration, and hypokalemia
Fanconi’s syndrome – total tubular dysfunction Inability to absorb everything including sugar and
protein
OTHER NOTES
Normal:
Figure 4: Normal
In diarrhea, loss of bicarbonate acidosis
Urine is acidic because dun motinataponang acids sa urine due to metabolic acidosis
If normal ang anion gap or no change in the level of the other anions, then the chloride ions will increase resulting to hyperchloremic metabolic acidosis. In non-diarrheal state but loss of bicarbonate then
the loss may be due in the urine (thus alkaloticyung urine mo) – also hyperchloremic metabolic acidosis If there is loss of bicarbonate but with normal anion
gap, then you will have hyperchloremic acidosis (kasiyung chlorine angtataas to maintain the balance)
Figure 5: Hyperchloremic Metabolic Acidosis
In sepsis:
Increased production of lactic acid increase yung other anions mo so the bicarbonate will decrease Hypo-anion gap metabolic acidosis (though di komagets kung bakit hypo, bastayunangsabini doc)
Figure 6: Hypo-anion gap metabolic acidosis
Diabetic ketoacidosis: Increase acid as ketone
High increase anion gap metabolic acidosis (di komagets kung bakitbastayansabini doc. Hehe) Vomiting
Loss of chloride increase bicarbonate alkalosis Hypochloremic metabolic alkalosis (also can be caused by loss of chloride ions in the urine due to poor reabsorption in the kidney)
Figure 7:Hypochloremic metabolic alkalosis
In normal anion gap, ang gagalaw lang ay ang bicarbonate and chloride ions. Normal means walang increase in other anions such as lactates, phosphates, sulfates, etc.
In either alkalosis or acidosis, you will have
dehydration because you are losing a lot of
electrolytes (osmotic diuresis). You also lose
potassium thus you will have hypokalemia manifested by weakness.
