Kidneys and Urinary Tract Disorders Flashcards

Question

When is acute-on-chronic renal failure suggested?

Answer 1

Acute-on-chronic renal failure is suggested by the child having faltering growth, anaemia, and disordered bone mineralization (renal osteodystrophy).

Answer 2

Non-specific symptoms such as sepsis, hypotension, decreased urine output, lower urinary tract symptoms or oedema Acute-on-chronic renal failure is suggested by: o Growth failure o Anaemia o Disordered bone mineralisation (renal osteodystrophy)

Answer 3

Serum creatinine Urine output GFR KDIGO criteria or pRIFLE

Answer 4

Serum creatinine Urine output GFR KDIGO criteria or pRIFLE

Answer 5

* Use **STOP AKI** * **Sepsis -** perform a septic screen * **Toxins -** identify and stop nephrotoxic drugs (e.g. NSAIDS, amino glycoside. iodine based contrast agents) * **Optimise** volume status and BP * Hypovolaemic - give bolus saline * Withhold diuretics * **Prevent** harm * Treat reversible causes e.g. urinary tract obstruction * Treat life threatening complications e.g. acidosis and hyperkalaemia **Pre-renal failure** o Due to hypovolaemia, decreased sodium excretion because the body is trying to retain it o Hypovolaemia should be urgently addressed with **fluid replacement** and circulatory support o **Dopamine/adrenaline** in severe hypotension o **Furosemide** if volume overloaded

Answer 6

AKI in childhood generally has a good prognosis unless it is complicating a more serious condition (e.g. severe infection, following cardiac surgery)

Answer 7

Affects 3-7% of girls and 1-2% of boys before age of 6 years o More common in boys until 3 months of age (dye to congenital abnormalities) and then much more common in girls 12-30% of them have recurrence within a year

Answer 8

May involve kidneys (pyelonephritis) - fever and systemic involvement or cystitis - no fever

Answer 9

Up to half of those affected have a structural abnormality of the urinary tract Pyelonephritis o Involves kidneys o Associated with fever and systemic involvement o May damage the growing kidney and form a scar, predisposing to hypertension and progressive CKD if scarring is bilateral

Answer 10

o Escherichia coli–most common (80%) o Klebsiella o Proteus ▪ More common in boys ▪ Predisposes to formation of phosphate stones (as it alkalises urine) o Pseudomonas ▪ Suggests that there may be some structural abnormality in urinary tract ▪ More common in children with plastic catheters or ureteric stents o Enterococcus faecalis

Answer 11

o Antenatally diagnosed renal or urinary tract abnormality o Incomplete bladder emptying due to infrequent voiding, vulvitis, hurried micturition, obstruction by a loaded rectum via constipation, neuropathic bladder o Vesicoureteric reflux (found in 35% of children presenting with UTI) o Poor hygiene e.g. not wiping from front to back in girls

Answer 12

Infants: non-specific symptoms o Fever o Vomiting o Lethargy/irritability o Poor feeding/faltering growth o Jaundice o Septicaemia o Offensiveurine o Febrile seizure (\> 6 months)

Answer 13

o Dysuria, frequency, urgency o Abdominal pain or loin tenderness o Fever+/-rigors o Lethargy and anorexia o Vomiting, diarrhoea o Haematuria o Offensive/cloudy urine o Febrile seizure o Recurrence of enuresis

Answer 14

• Test urine sample in any infant/child presenting with o Unexplained fever \> 38 degrees o An alternative site of infection who remain unwell despite treatment o Symptoms and signs suggestive of UTI o Collection of urine samples ▪ Children in nappies BEST METHOD: a ‘clean-catch’ sample into a waiting clean pot when nappy is removed If not possible, use urine collection pad Adhesive plastic bag applied to perineum after careful washing (possible contamination) Urethral catheter if urgent, and no urine is passed Suprapubic aspiration (fine needle attached to syringe inserted directly into a bladder under US guidance) if severely ill and non-invasive methods not possible ▪ Older children • MIDSTREAM SAMPLE, with careful cleaning and collection to avoid contamination o Send sample for microscopy and culture ▪ **A bacterial culture of \> 10⁵ colony-forming units (CFU) of a single organism per millilitre** in a properly collected specimen gives a 90% probability of infection ▪ If mixed growth of organisms→suggests contamination Urine dipstick o Can be used as screening test o Culture should still be performed unless both leucocyte esterase and nitrite are negative, or is clinical symptoms and dipstick tests do not correlate o Assess risk of serious illness (ABCDE) ▪ Temperature ▪ Respiratory rate ▪ Heart rate ▪ Do not delay treatment in a child with high risk of serious illness if urine sample cannot be obtained ▪ Capillary refill time ▪ Check for signs of dehydration

Answer 15

The extent of further investigation beyond urine sample is controversial as they can be invasive o There has been a move away from extensive investigation of all children with UTIs to those with atypical or recurrent UTIs o Atypical UTIs include ▪ Seriously ill or septicaemia ▪ Poor urine flow ▪ Abdominal or bladder mass ▪ Raised creatinine ▪ Failure to respond to suitable antibiotics within 48 hours ▪ Infection with atypical organisms o An initial ultrasound will identify serious structural abnormalities and urinary obstruction and renal defects o If urethral obstruction is suspected, MCUG should be performed promptly o NOTE: functional scans should be deferred for 3 months after a UTI, unless the ultrasound is suggestive of obstruction, to avoid missing a new scar and because false-positive results may be produced due to transient inflammation o NICE guidelines on further investigations: ▪ Infants and children with atypical UTI should have an ultrasound of the urinary tract to identify structural abnormalities ▪ DMSA and MCUG may also be performed in children \< 6 months presenting with atypical or recurrent UTI DMSA to check for renal scars 3 months after UTI MCUG or MAG3 to detect obstruction and VUR

Answer 16

If both leucocyte esterase + nitrite positive: treat as UTI (+ send urine for culture if \< 3 years, suspicion of pyelonephritis, no response to treatment etc) If both leucocyte esterase + nitrite negative: UTI unlikely, consider DDx If leucocyte esterase positive + nitrite negative: o Send urine sample for microscopy and culture o If \< 3 years: start antibiotic treatment o If \> 3 years: only start abx if good clinical evidence of UTI • If leucocyte esterase negative + nitrite positive: treat as UTI o Start abx if dipstick was with a fresh urine sample o Send urine for culture to confirm

Answer 17

Definition: *normal micturition occurring at an inappropriate or socially unacceptable time or place, occurring after a developmental age when bladder control should be established (~5 years)*

Answer 18

* Day and night: 5 yr * Day only: 4 yrs

Answer 19

nocturnal enuresis in which the child has never had a period of dryness longer than 6 months

Answer 20

nocturnal enuresis recurring after a period of more than 6 months of the child being dry at night

Answer 21

*Lack of bladder control during the day in a child old enough to be continent ( over the age of 3-5 yrs)*

Answer 22

Nocturnal enuresis \> 2 nights/week is present in 6% of 5 yr olds 1.5% of 10yr olds. M\>F by 2:1

Answer 23

Dependent on the development of 2 functions: 1. Ability of bladder to increase in functional capacity, aided by the action of ADH to decrease nocturnal urine production. 2. The arousal of the individual to the stimulus provided by a full bladder.

Answer 24

* Genetically determined delay in acquiring night time dryness, with ⅔ have affected **first degree relative** * Young children also need reasonable freedom from **stress** and a measure of **potential approval** to lear night time continence * **Emotional stress** can interfere and cause secondary nocturnal enuresis * Most children with nocturnal enuresis are psychologically normal and tx relies on symptomatic approach

Answer 25

* UTI * Constipation with faecal impaction severe enough to lower bladder volume and cause bladder neck dysplasia * Polyuria with osmotic diuretics e.g. DM or renal concentrating disorders CKD * Overactive bladder * Structural abnormalities e.g. ectopic ureter or near abnormalities

Answer 26

• Investigations for secondary NE o Urine dipstick to check for infection, glycosuria and proteinuria o Assessment of urine concentrating ability by measuring osmolality of an early morning urine sample o Ultrasound of the renal tract

Answer 27

Explain: * Common problem * Beyond conscious control of child - no blame * No punishment * Fluid can be restricted 2 hrs before bed o Children \< 5 years * Reassure the parents that many children aged \< 5 yrs wet the bed and this usually resolves without intervention * Ensure easy access to the toilet at night (e.g. potty near the bed) * Encourage bladder emptying before bed * Consider a positive reward system * Star chart o Children \> 5years * If bedwetting is infrequent (\< 2 per week) reassure the parents and offer watch- and-see approach * Can use a star or reward chart * Don’t punish or make the child feel embarrassed If long-term treatment is required, offer: **1st line: enuresis alarm** with positive reward system - ⅓ relapse 2nd line: desmopressin o Note: fluid should be restricted 1 hour before desmopressin until 8 hours after o May need to use detrusor-relaxing drugs if have nocturnally overactive bladder If rapid or short-term control is required (e.g. school trips), offer desmopressin If bedwetting recurs following treatment, restart previously successful treatments and offer combination treatment with desmopressin and an enuresis alarm Referral If bedwetting has NOT responded to two courses of treatment, refer to secondary care, enuresis clinic or community paediatrician Self-help group: Advice + assistance parents e.g. Eric, The children Bowel + Bladder Charity

Answer 28

Refer all children to secondary care or an enuresis clinic Also: * Exclude neuro causes * Constipation should be treated * Small portable alarm for lack of attention to bladder * Anticholinergics - **oxybutin** - dampens down bladder contractions if other measure fail

Answer 29

o Lack of attention to bladder sensation (manifestation of developmental or psychogenic problem) o Detrusor instability (sudden, urgent urge to void induced by sudden bladder contractions) o Bladder neck weakness o Neuropathic bladder (bladder is enlarged and fails to empty properly, irregularly thick wall, associated with spina bifida and other neurological conditions) o UTI o Constipation o Ectopic ureter (causes constant dribbling)

Answer 30

* May reveal evidence of neuropathic bladder i.e. bladder distension, abnormal perineal sensation, anal tone, or abnormal leg reflexes, gait * Sensory loss in distribution of S2,S3 and S4 dermatome * Spinal lesion may be present * Girls who get up to pool of urine due to ectopic ureter into vagina

Answer 31

• Investigations o Urine should be sent for MC&S o Ultrasound may reveal abnormalities o Urodynamic studies may be required o MRI may be used to exclude a spinal defect

Answer 32

• The loss of previously achieved urinary continence may be due to: o Emotional upset (MOST COMMON) o UTI o Polyuria from an osmotic diuresis (e.g. diabetes mellitus, diabetes insipidus, CKD)

Answer 33

Investigations o Urine dipstick to check for infection, glycosuria and proteinuria o Assessment of urine concentrating ability by measuring osmolality of an early morning urine sample o Ultrasound of the renal tract

Answer 34

o The following underlying causes can be managed in primary care ▪ UTI ▪ Constipation o The following underlying causes are likely to need specialist referral ▪ Diabetes ▪ Recurrent UTI ▪ Psychological problems ▪ Family problems ▪ Developmental, attention or learning difficulties ▪ Known or suspected physical or neurological problems

Answer 35

Summary o Look for possible causes (e.g. constipation, diabetes) o **BED** * *Behavioral** - Advise onreduced fluid intake before bed, diet and toileting behaviour & Reward systems (e.g. star charts) * *Enuresis** alarm * *Desmopressin**: may be used 1st line if \> 7 years or if short-term control is needed (e.g. holiday)

Answer 36

Most common vasculitis of childhood Affects small vessels Involves tissue deposition of IgA-containing immune complexes within affected organs

Answer 37

o Characteristic purpuric rash over extensor surfaces (esp buttocks and legs) o Arthralgia o Abdominal pain o Periarticular oedema o Glomerulonephritis

Answer 38

o Usually affects ages 3-10 years o More common in boys (2:1) o Peaks during winter months, often preceded by an upper RTI

Answer 39

o Underlying aetiology is unknown – thought to be an immune-mediated vasculitis o Possible theory: genetic predisposition and antigen exposure increase circulating IgA levels and disrupt IgG synthesis→ the IgA and IgG interact to produce complexes that activate complement and are deposited in affected organs precipitating an inflammatory response and vasculitis o Similar pathophysiology to IgA nephropathy

Answer 40

**H**aematuria **S**urface rash on extensors (non- blanching raised palpable purpura), **S**crotal Swelling **P**olyarthritis, Abdo **P**ain Fever Rash o Symmetrically distributed over the buttocks and extensor surfaces of arms and legs o Trunk is usually spared o Usually palpable o First clinical feature in about 50% of cases • Joint pain o Particularly knees and ankles - ⅔ of pts o Accompanied by periarticular oedema • Colicky abdominal pain o Can be treated with corticosteroids o Can cause haematemesis and melaena - intussusception can occur • Renal involvement o Over 80% have haematuria or mild proteinuria o Usually, a complete recovery is achieved o Persistent haematuria or proteinuria is a risk factor for progressive CKD RFs for CKD: * Heavy proteinuria * Oedema * Hypertension * Deteriorating renal function o So, all children with HSP should be followed for a year

Answer 41

Urinalysis→RBCs, proteinuria, casts 24-hour urine collection for protein Serum creatinine and electrolyte levels – to assess for renal failure Serum IgA – raised Coagulation studies – normal Skin biopsy – IgA deposition Renal biopsy – IgA, C3 and fibrin deposition in the mesangial region

Answer 42

Most cases will **resolve spontaneously** within _4 weeks_ Admit if inability to maintain adequate hydration with oral intake, severe abdominal pain, severe renal involvement etc o If dehydrated→IV fluids o If significant anaemia→may need RBC transfusion Joint pain can be managed using **paracetamol or ibuprofen** If there is scrotal involvement or severe oedema or severe abdominal pain, **oral prednisolone** may be given - also rest, hydration, and elevation of affected area **IV corticosteroids** are recommended in patients with nephrotic-range proteinuria and those with declining renal function In rapidly progressive nephritis: **IV corticosteroid + oral prednisolone + cylophosphamine -** renal transplant and dialysis may be considered. Renal transplant may be considered in end-stage renal disease Follow up for BP and renal function

Answer 43

Characterised by a triad of o PROTEINURIA (\> 50mg/kg/24 hours OR urine PC ratio \> 300mg/mmol) ``` o HYPOALBUMINAEMIA(\<30g/L) o PERIPHERAL OEDEMA ```

Answer 44

Cause is unknown but some cases occur secondary to systemic diseases e.g. Henoch-Scholein purpura and other vasculitides, SLE, infections (e.g. malaria), allergens (e.g. bee sting) 80% of cases are due to MINIMAL CHANGE GLOMERULONEPHRITIS

Answer 45

Pathophysiology o Glomeruli are damaged and become more permeable, allowing plasma proteins to pass through leading to proteinuria o Albumin is one of the proteins hence you get hypoalbuminaemia o This causes peripheral and periorbital oedema as there is less oncotic pressure in blood vessels and fluid leaks out

Answer 46

Other features o Hyperlipidaemia o Hypercoagulable state – due to loss of antithrombin III o Predisposition to infection – due to loss of Ig

Answer 47

* Periorbital oedema (particularly on waking) – usually the earliest sign * Scrotal or vulva, leg and ankle oedema * Ascites * Breathlessness due to pleural effusion and abdominal distension * Infection such as peritonitis, septic arthritis or sepsis due to loss of protective immunoglobulins in the urine

Answer 48

• **Urine protein (dipstick) -** 24 hour urine collection can also be done FBC and ESR - for infection and increased Hb also suggests intravascular fluid depletion Urea, electrolytes, creatinine, **albumin -** Low Na+, high urea and/or high creatinine → intravascular fluid depletion Complement levels: C3 and C4 - low C3- post infectious glomerulonephritis, if low C3 + C4 - SLE Antistreptolysin O or anti-DNAase B titres and throat swab (for post-streptococcal glomerulonephritis) Urine microscopy and culture Urinary sodium concentration - Low (\<10mmol/L) - intravascular fluid depletion Hepatitis B and C screen - looking for cause Malaria screen if travel abroad

Answer 49

Steroid-sensitive nephrotic syndrome

Answer 50

Accounts for 90% of nephrotic syndrome in children. More common in boys, Asian ethnicity, and associated with atopy Tends to affect ages 1-10 Often precipitated by respiratory infections, recent vaccination or by immune stimulus (e.g. bee sting)

Answer 51

o T cells in the blood release cytokines-glomerular-permeability factor which specifically damages the foot processes of the podocytes making them flatter (effacement) o Damaged foot processes lose their negatively charged coat→allow negatively charged molecules like albumin to go through o Note: in minimal change disease, there is SELECTIVE proteinuria – larger proteins like immunoglobulins are not filtered through (unlike other causes of nephrotic syndrome)

Answer 52

Investigations will show o No macroscopic haematuria o Normal blood pressure o Normal complement levels o Normal renal function o Renal biopsy and histology ▪ Light microscopy: will be NORMAL (hence minimal change disease) ▪ Electron microscopy: effacement of podocyte foot processes/fusion of podocytes seen ▪ Immunofluorescence is negative

Answer 53

* 20% - resolve directly * 30% - infrequent relapses * 50% - frequent relapses (steroid-dependent) - urine test at home

Answer 54

• Hypovolaemia o As the oedema forms, the intravascular compartment may become depleted o The child may complain of abdominal pain and feel faint o The body will respond with peripheral vasoconstriction and urinary sodium retention o Low urine sodium (\< 10 mmol/L) and high haematocrit are suggestive of hypovolaemia o TREATMENT: IV 0.9% saline o If severe, IV 20% albumin infusion with furosemide may be needed (NOTE: this can precipitate pulmonary oedema and hypertension from fluid overload, and the diuretics could worsen the hypovolaemia) • Thrombosis o Hypercoagulable state results from: ▪ Urinary losses of antithrombin III ▪ Thrombocytosis (may be worsened by steroid therapy) ▪ Increased synthesis of clotting factors ▪ Increased blood viscosity from raised haematocrit • Infection o High risk of infection by capsulated bacteria (especially *Pneumococcus*) as immunoglobulins are also lost through urine o Pneumococcal and seasonal influenza vaccination is recommended o Chickenpox and shingles should be treated with aciclovir • Hypercholesterolaemia o Correlates inversely with serum albumin o Cause is unknown

Answer 55

* Focal segmental glomerulosclerosis * ▪ Most common * ▪ Familial or idiopathic * ▪ Prognosis * 30% progress to end-stage renal failure in 5 years * 20% respond to cyclophosphamide, cyclosporin, tacrolimus or rituximab * Recurrence post-transplant is common * o Mesangiocapillary glomerulonephritis (membranoproliferative glomerulonephritis) ▪ More common in older children * Haematuria * Low complement levels * Decline in renal function over many years * o Membranous nephropathy * ▪ Associated with hepatitis B * ▪ May precede SLE * ▪ Most remit spontaneously within 5 years

Answer 56

o Refer to paediatric nephrologist o Management of oedema using diuretic therapy, salt restriction, ACEi and sometimes NSAIDs (which may reduce proteinuria) o Genetic testing is available and helps direct management e.g. withdrawal of immunosuppression or supplementation of CoQ10 if CoQ10 pathway defect

Answer 57

Presents in first 3 months of life Rare - genetic testing recommended - 70% have an underlying genetic defect More common in Finns and in consanguineous families Associated with high mortality due to complications of hypoalbuminaemia (intensive nutritional management better) Management: may need unilateral nephrectomy (to manage albuminuria) and subsequent dialysis, definitive treatment by renal transplantation

Answer 58

▪ Multicystic kidney ▪ Compensatory hypertrophy ▪ Obstructed hydronephrosis ▪ Renal tumour (Wilms tumour) ▪ Renal vein thrombosis

Answer 59

▪ Polycystic kidneys (autosomal dominant + autosomal recessive) ▪ Tuberous sclerosis ▪ Renal vein thrombosis

Answer 60

Presence of crystalline stones (calculi) within the urinary system (kidneys and ureters)

Answer 61

UNCOMMON in childhood

Answer 62

The MOST COMMON type of stone are phosphate stones, which are associated with infection (*Proteus*)

Answer 63

Calcium-containing stones may occur with idiopathic hypercalciuria, increased urinary urate and oxalate excretion

Answer 64

o UTI o Structural anomalies of the urinary tract o Metabolicabnormalities

Answer 65

Nephrocalcinosis (depositions of calcium in the parenchyma) may occur in hypercalciuria, hyperoxaluria and distal renal tubular acidosis This may be a complication of furosemide therapy in neonates

Answer 66

Haematuria Loin or abdominal pain UTI Passage of a stone

Answer 67

* Urine dipstick: for microscopic haematuria * Non-contrast CT (gold-standard) * U&Es and creatinine to check renal function

Answer 68

1. Conservative management with **IV fluids**, **analgesia** (morphine) and **anti-emetics** (ondansetron) 2. **Bacterial Infection** - antibiotic treatment with **co-trimoxazole** or **nitrofurantoin**, or surgical decompression 3. **Small stones** - medical expulsive therapy 1. May pass naturally 2. Tamsulosin OR Alfuzosin OR Silodosin 4. Larger stones and those that do not pass spontaneously - surgical removal 1. 1st line: ESWL (extracorporeal shock wave lithotripsy or ureteroscopy 5. High fluid intake is recommended in all affected children Further ix for structural abnormalities

Answer 69

HUS is a triad of o Microangiopathic haemolytic anaemia (MAHA): intravascular haemolysis and red cell fragmentation o Acute renal failure o Thrombocytopenia

Answer 70

o D+: diarrhoea-associated (prodrome of diarrhoea) ▪ More common in young children o D-: no prodromal illness identified

Answer 71

Typical HUS is secondary to GI infection with E coli O157:H7 o Acquired through contact with farm animals or eating uncooked beef o Produces verocytotoxin that enters GI mucosa and attacks endothelial cells, where it causes intravascular thrombogenesis Less often caused by Shigella

Answer 72

o A toxin causes endothelial damage which leads to platelet activation o Endothelial injury results in platelet aggregation and the release of unusually large vWF multimers and activation of platelets and clotting cascade o There is also fibrin deposition in small vessels leading to microthrombi o Damaged RBCs clog up vessels ▪ The glomerular afferent arteriole and capillaries are particularly vulnerable (undergo fibrosis necrosis) ▪ This leads to renal ischaemia and acute renal failure o The thrombi also promote intravascular haemolysis o MAHA results from damage to RBCs

Answer 73

• GI prodromal illness o Severe abdominal colic o Watery diarrhoea that becomes bloodstained • General o Malaise o Fatigue o Nausea o May have fever • Renal o Oliguria or anuria o Haematuria

Answer 74

• FBC o Normocyticanaemia o High neutrophils o Very low platelets • U&Es o High urea o High creatinine o High K+ o Low Na+ **Clotting: normal (DIC does not usually occur)** LFTs o **High unconjugated bilirubin** o **High LDH** from haemolysis Blood cultures ABG: low pH, low bicarbonate, low PaCO2, normal anion gap Blood film: schistocytes, high reticulocytes and spherocytes Urinalysis Stool samples: MC&S

Answer 75

* Consult nephrology and haematology specialists * Children with the typical presentation should be admitted * Supportive * Monitor urine output and fluid balance * **In diarrhoea HUS(D+HUS) use of antibiotics can worsen disease** * Maintain adequate hydration status (avoid cardiopulmonary overload) – **IV isotonic crystalloids** * Monitor blood pressure (treat If elevated) * Treatment should be with CCBs (ACE inhibitors can reduce renal perfusion) * If anaemic, **red cell transfusion** is needed * Avoid antibiotics, anti-diarrhoeals, narcotic opioids and NSAIDs * 50% of patients will require **dialysis** in the acute phase * If irreversible renal failure has occurred then **renal transplant** will be needed * **Long-term follow-up** is necessary because there may be persistent proteinuria and the * development of hypertension and progressive CKD * **Atypical HUS** has no diarrhoeal prodrome, may be familial and frequently relapses * This has a high risk of hypertension and progressive CKD with a high mortality * **Thrombotic thrombocytopenic purpura** will require plasmapheresis

Answer 76

CKD is the progressive loss of renal function that can be caused by many conditions

Answer 77

Congenital and familial causes are more common in childhood than acquired diseases o Commonest cause: structural malformations and hereditary nephropathies o Renal dysplasia +/-reflux o Obstructive uropathy o Glomerular disease o Congenital nephrotic syndrome o Tubulointerstitial diseases o Renovascular disease o Polycystic kidney disease o Metabolic

Answer 78

• CLINICAL FEATURES (of stage 4/5 CKD): o Anorexia and lethargy o Polydipsia and polyuria o Faltering growth/growth failure o Bony deformities from renal osteodystrophy o Hypertension o Acute-on-chronic renal failure (precipitated by infection or dehydration) o Incidental finding of proteinuria o Unexplained normochromic, normocytic anaemia Symptoms before these stages unlikely Many children will have had their renal disease detected antenatally

Answer 79

The aims of management are to prevent the symptoms and metabolic abnormalities of chronic kidney disease, to allow normal growth and development, and to preserve residual renal function. The management of these children should be conducted in a specialist paediatric nephrology centre.

Answer 80

o Erythropoietin stimulating agent can be used o **Iron supplementation** should also be given

Answer 81

o Decreased activation of vitamin D leads to phosphate retention and hypocalcaemia, which, in turn, leads to secondary hyperparathyroidism and eventually **osteitis fibrosa cystica** and **osteomalacia** o Phosphate restriction (by reducing milk), using **calcium carbonate** as a phosphate binder and **activated vitamin D** supplements can help

Answer 82

o Many children will also have obligatory loss of salt and water o They need salt supplements and a lot of water o Treatment with bicarbonate supplements is needed to prevent acidosis

Answer 83

o Anorexia and vomiting are common o Calorie supplements or NG/gastrostomy feeding is often necessary to optimise growth o Protein intake should be sufficient to maintain growth and normal albumin (but preventing the accumulation of toxic metabolic by-products)

Answer 84

o Growth hormone resistance, characterised by a high GH level but poor growth, is a feature of CKD o Recombinant human GH is effective in improving growth for up to 5 years of use o Many children with stage 4/5 CKD will have delayed puberty or subnormal pubertal growth spurt

Answer 85

* Medical * Diet * Complications: * Anaemia * Secondary hyperparathyroidism * Metabolic acidosis * Salt and water loss * Hormonal abnormalities

Kidneys and Urinary Tract Disorders Flashcards

(117 cards)