Red urine

Hemoglobinuria Myoglobinuria Drugs (rifampicin),food Inborn errors of metabolism(porphyria) Urate crystals Hematuria Do dipstick,microscopy (>5cells/ul in

fresh uncentrifuged urine, >3 cells/HPF in centrifuged sediment.

Red if fresh(bladder), or brown color as Hb converted to acid haematin by urinary acids

Early hematuria:urethral cause Terminal hematuria:bladder cause Microscopy:dysmprhic RBC,RBC

cast:glomerular bleeding Prevelance of .5-1.6% in school children

RBC casts

RBC casts

History

Fever,urinary symptoms….infection Colicky loin pain,lower tract

symptoms…..renal calculus Rash,arthritis…HSP,SLE Preceding URTI…..PSGN,IgA nephropathy Coagulopathy,trauma,tumor,exercise FH of hematuria,deafness,renal failure…

Alport O/E:HTN,kidneys,genitalia,rash

Investigations

Urine protein/creat ratio EUC,albumin ASOT,C3,C4,ANA FBC,clotting studies Urine calcium/creat ratio U/S ,XRAY,CT Urine analysis on parents IgA,cystoscopy Renal biobsy

Macroscopic hematuria

Most common cause is infection,then perineal irritation,trauma

Viral infections,adenovirus 11,12 may cause hemorrhagic cystitis

Exercise induced hematuria not associated with renal disease.

Recurrent gross hematuria as IgA nephropathy,Alport,nut cracker (thin,loin pain,compression of renal vein bet aorta,SMA

Causes of hematuria

1.Glomerular causes Familial benign hematuria GN:primary as postinfectious,MPGN,IgA

nephropathy secondary GN as SLE,HSP. HUS,interstital nephritis,renal vein

thrombosis,cystic renal disease Alport

Non glomerular causes UTI Hypercalcuria,renal calculi Trauma,exercise Coagulpathy as sickle Vascular malformations Nut cracker syndrome Menarche Malignancy as nephroblastoma of the

kidney or bladder tumors

Persistent MA without proteinuria : 1.Beningn familial hematuria 2.idiopathic hypercalcuria 3.IgA nephropathy 4.Alport syndrome

Persistent MA without proteinuria : 1.Beningn familial hematuria 2.idiopathic hypercalcuria 3.IgA nephropathy 4.Alport syndrome

Alport Syndrome

80% XL,20% AR

Renal failure,sensorineural deafness higher frequencies,ocular changes(anterior lenticonus,retinal changes

Present as micro and rarely macroscopic hematauria with URTI

Proteinura,HTN later age

Diagnosis by EM:Thinning of GBM,split and duplicated lamina densa,basket weave

Males progress to ESRD,deafness by 30y

ACEI may delay progression to ESRD

Defiency of α5 of type 4 collagen

Benign Familial Hematuria(TBMN)

AD inheritance Present as microscopic

hematuria,no proteinuria or renal failure

EM:thinning of GBM Follow up for proteinuria,HTN

GBM in Alport syndrome

GBM in Alport syndrome

IgA nephropathy

Recurrent macroscopic hematuria,loin pain 1-2 days following URTI,last < 3 days.

Persistent microscopic hematuria ±proteinuria

Nephritic,nephrotic syndrome rare

Present second decade,more in males

Familial cases reported IgA high in 35-50% Diagnosis:LM:focal or diffuse mesangial cell

proliferation,expansion of mesangial matrix IM:IgA,C3 deposits Prognosis for children better than adults Young children without macroscopic

hematuria have the best long term outcome

Heavy proteinuria is a risk factor for progression to ESKD.

Progression to ESRD is slow(25% need dialysis in 20y)

Children with nephrotic syndrome are treated with steriods

ACEI are used to delay progression,decrease proteinuria

Fish oil

IF showing mesangial depostis

Normal glomerulus

IgA deposits

Thin glomerular basement membrane disease

PROTEINURIA

DIPSTICK values .trace (.15g/l),+1 (.3g/l),+2 (1g/l),+3 (3g/l),+4

(20g/l)

False postive when urine concentarted,alkaline urine

Children excrete 150 mg/day of protein or 60-240 mg/m2/day

40 % of normal urinary protein is tissue rather than plasma as tamm-horsfall (a gp secreted in TALH )

Almost of the flitered smaller proteinare absorbed in the proximal CT.

Protein-creatinine ratio to estimate protein excretion

Urine protein/creat ratio correlates with measurement of protein in 24 hour collection.

Most normal subjects have a ratio below.02 mg/umole (.2g/g) in above 2y,.05 in children 6-24 m

Micoalbuminuria ranges 30-300 mg albumin/g creat

B2-microglobulin in urine indicates proximal tubular injury

Classification 1-Functional:seen in

stress,fever,cold,exercise,CHF

2-Idiopathic transient or intermittent

3-postural:in adolesents,males,less than 2g/day,proteinuria in upright position but not when recumbent

Decrease in amount with age Has a good outcome

4-pathologic:increase permeability of GBM,loss of anions(nephrotic,GN)

Loss of nephron mass:single kid,cystic disease from hyperfilteration

secretory,overflow:UTI,in newborns as tam