PEDIA 4.1 Nephrology

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

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KIDNEY AND URINARY TRACT KIDNEYS  Nephron  Glomerulus  Tubules - Calyces  Interstitium  Special Cells

II. URETER III. URINARY BLADDER  Urinary Bladder Junction  Urethral Valve/ Sphincter

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

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  Valve function which is junction 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

URINE FORMATION  Initiated by elaboration of a large volume of proteinfree 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  Acidification takes place

Page 1 of 7 Jam, Richelle, April, Anne

 Vascular Imaging o Angiogram o Echoangiogram  Scan o Technetium Scan o CT-Scan –anatomic o Magnetic Resonance Imaging (MRI) – vascular and anatomic

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  Overcrowding/ inflammation →oliguria/anuria

 Responsible for increased urine concentration  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

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

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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 xray 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.

PEDIA_IV.1 Nephrology

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 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 Page 2 of 7

 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

PEDIA_IV.1 Nephrology

 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  Remaining nephrons are overworked Page 3 of 7

REFLUX GRADING

immune complexes

 Occurs AFTER strep infection→ PSAGN

  Figure 2. Reflux grading (Nelson) GRADE Grade 1 Grade 2

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Grade 3

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Grade 4 Grade 5

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Table 3.Reflux Grading DESCRIPTION Reflux into a nondilated ureter Reflux into the upper collecting system without dilation Reflux into a dilated ureter and/or blunting of calycealfornices Reflux into a grossly dilated ureter Massive Reflux with significant dilatation and tortuosity and loss of capillary impression

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4. 5. 6.

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WHAT TO DO WITH PYELONEPHRITIS: VESICOURETERAL REFLUX 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 Reflux repair by re-implantation of ureter by urologist 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 Health status monitoring a. Renal function b. Anthropometric evaluation Follow-up imaging a. For anatomic changes – scar formation b. For determination of functional status 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

PEDIA_IV.1 Nephrology

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 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

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Table 4. Comparison between UTI and PSAGN UTI PSAGN Increased WBC shown in  Increased RBC urinalysis Usually involves tubules,  Involves the glomerulus interstitium + Protein  + Protein, small amounts Sepsis and Scar  Good recovery in 6 to 8 weeks Normal volume of urine  May involve Oliguria and pyuria

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Hematuria Oliguria Edema Hypertension

Acute Stage = 7-14 days

Gross to microscopic hematuria (minus edema and hypertension

Diuretic Stage

 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

Microscopic hematuria

Variants: 1. Chronic glomerulonephritis 2. Rapidly progressive glomerulonephritis (RPGN)

Recovery or Convalescent Stage

Complete Recovery: 8 weeks average (6 mos to 1 year)

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 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

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 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

PEDIA_IV.1 Nephrology

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  Pan-tubular dysfunction

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OTHER NOTES Normal:

 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 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 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 5: Hyperchloremic Metabolic Acidosis 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.

PEDIA_IV.1 Nephrology

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