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Hematuria and Renal Failure BY: Prof. Jameela Kari: CABP, MD, CCST, FRCPCH, FRCP (UK) Professor of Paediatric Nephrology Dr. Salah Al- Morshedy : M.D.& lecturer of Pediatric Nephrology. Learning objectives :. By the end of this lecture, you should know about : Hematuria

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Hematuria and Renal Failure BY:Prof.Jameela Kari:CABP, MD, CCST, FRCPCH,FRCP (UK)Professor of Paediatric NephrologyDr.Salah Al-Morshedy :M.D.& lecturer of Pediatric Nephrology

learning objectives
Learning objectives:

By the end of this lecture, you should know about :Hematuria

1-Define hematuria.

2-List types of hematuria.

3-Recognize cause of microscopic hematuria.

4-Recognize cause of macroscopic hematuria.

5-Discuss investigation of hematuria.

learning objectives3
Learning objectives:

Renal Failure

1-Define Renal Failure.

2-Differentiate between ARF and CRF.

3-Discuss causes of ARF.

4-Recognize the clinical presentation of ARF.

5-Discuss the diagnostic test of ARF.

6-Recognize clinical presentation of CRF.

7-Discuss the diagnostic test of CRF.

8-Describe the management of ARF and CRF.

content of the lecture
Content of the lecture:


Diagramatic explanation of renal system.

causes of hematuria (glumerulus and non glumerulus)

Non-renal (systemic) causes.

Stepwise approach for investigation.


content of the lecture5
Content of the lecture:

Renal Failure

Definition of R.F.

difference between ARF and CRF.

Explain how to differentiate between Pre-renal, renal and post-renal causes in ARF.

Investigation of ARF and CRF.

Management of ARF and CRF.

renal system
  • Investigation of renal system
  • Haematuria/ PSGN
  • Proteinuria/ Nephrotic syndrome
  • UTI
  • Congenital Anomalies
investigation of the renal system
Investigation of the renal system
  • Urine analysis
  • Urine electrolytes: fraction excretion of sodium (pre-renal <1%, renal >1-2%)
  • 24 hours urine for protein, Ca etc
  • GFR(creatinine clearance= ml/1.73m2/minute)
  • Cultures: older children: midstream

Younger children:SPA, Catheter, Bag

  • Imaging: US, KUB/IVU, MCUG, CT scan, isotope scan (DMSA, DTPA)
  • Renal biopsy
  • Macroscopic = frank = gross
  • Microscopic > 5 RBCs per high powered field
  • Red urine:
    • Blood (RBCs= haematuria, haemoglobin= haemoglobinuria)
    • Myoglobin
    • Food: blackberries
    • Aniline dyes used for coloring candy
    • Drugs: Rifampicin, phenolphthalein
    • Urate
    • Porphyrins
  • Glomerular: brownish or cola-coloured and may contain RBCs cast, proteinuria
  • Lower urinary tract: red to pink color urine and may contain clots
  • Haematological: thrombocytopaenia, DIC, coagulopathies, renal vein thrombosis, SCD
  • Glomerular: brownish or cola-coloured and may contain RBCs cast, proteinuria
  • Stones and hypercalciuria
  • Infection: bacterial, TB, viral
  • Lower urinary tract: red to pink color urine and may contain clots
  • Anatomic abnormalities: congenital, trauma, polycystic kidneys, tumors, vascular abnormalities
  • Exercise and drugs
glomerular diseases
Glomerular Diseases
  • 7 years old boy
  • Frank haematuria (smokey or tea colored)
  • H/O throat infection 2 weeks ago
  • O/E peri-orbital edema, BP 140/90 (hypertension)
    • What is the most likely diagnosis
    • What investigations
post streptococcal glomerulonephritis
Post-streptococcal glomerulonephritis:
  • Rare before the age of 3 years
  • Nephritic picture: Gross haematuria, edema , hypertension, renal insufficiency (normal RF-ARF)
  • Complications of hypertension: encephalopathy, congestive heart failure
  • Rarely: nephritic- nephrotic picture.
  • Urine analysis: RBCs, RBCs cast, proteinuria
  • Low complement C3
  • Evidence of streptococcal infection: throat culture, ASO titer and DNase B antigen and streptozyme test
  • Mild normochromic anaemia
  • Renal function

ARF  volume overload, hypertension, fits, hyperkalemia, hyperphosphatemia, hypocalcaemia and acidosis



Management of ARF

  • Complete recovery 95%
  • Infrequently: severe acute phase leading to chronic renal insufficiency
  • Recurrence are extremely rare
RBCs cast

Glomerulonephritis or vasculitis

Exclude extra-renal disorders

glomerular diseases20
Glomerular Diseases
  • MPGN
  • Rapidly progressive glomerulonephritits
  • SLE
  • Shunt nephritis
  • Goodpasture disease
  • Membranous
  • Anaphlactoid purpura
  • IgA nephropathy
  • Idiopathic (benign familial)
  • Alport syndrome
evaluation of a child with haematuria
  • History
  • Examination
  • Investigation:
    • Studies performed in all patients:
      • urine microscopy and culture
      • CBC
      • serum creatinine
      • serum C3 level
      • US kidneys
      • urine protein = urine albumin/creatinine ratio
      • calcium = urine calcium/creatinine ratio
Studies performed in selected patients:

Dnase B titer or streptozyme < 6 months duration

Skin or throat culture

ANA titer

Urine analysis looking for cast

Coagulation study/ platelet count

Sickle cell screen in black patients


Renal biopsy

Microscopic haematuria plus any of the following:

Diminished renal function


Persistant microscopic haematuria (>1 year)

Second episode of gross haematuria


Pink o microscopic haematuria, dysuria and sterile urine culture

case history
Case History:
  • 5 years old boy
  • Generalized malaise, abdominal pain, joints pain, peri orbital oedoma
henoch sch nlein purpura or anaphylactoid purpura
Henoch-Schönlein Purpura or (Anaphylactoid Purpura)
  • Renal involvement occurs in 25–50% of children during the acute phase
  • Haematuria with or without casts or proteinuria during the first few weeks of illness
  • The nephrotic syndrome, moderate azotemia, hypertension, oliguria, and hypertensive encephalopathy may occasionally occur.
  • Most children with renal involvement recover
recurrent gross haematuria or persistent microscopic haematuria
Recurrent Gross Haematuria or Persistent Microscopic Haematuria
  • IgA nephropathy (Berger)
  • Alport syndrome
  • Familial idiopathic haematuria
  • Idiopathic hypercalciuria.
iga nephropathy berger
IgA Nephropathy (Berger)
  • Glomerulonephritis with IgA as the predominant immunoglobulin in mesangial deposits, in the absence of any systemic disease
  • Haematuria + minimal proteinuria
  • Normal C3 + usually normal RF
  • Diagnosis: renal biopsy
iga nephropathy berger29
IgA Nephropathy (Berger)
  • Treatment: supportive
  • Prognosis: mainly good, only 30% has progressive disease:hypertension, diminished renal function, or proteinuria exceeding 1 g/24 hr between episodes of gross hematuria
alport syndrome
ALPORT Syndrome.
  • Hereditary nephritis.
  • Haematuria + proeinuria + sensorineural hearing loss (minority) + eye abnormalitie (10%).
  • Diagnosis: renal biopsy.
  • Males with Alport syndrome commonly develop end-stage renal failure in the 2nd or 3rd decade of life, occasionally in association with hearing loss. Females usually have a normal life span and only subclinical hearing loss.
idiopathic familial benign haematuria
Idiopathic Familial Benign Haematuria
  • No proteinuria
  • All investigations normal
  • Urine test of the parents and siblings
  • An excellent prognosis, but long-term follow-up is required to exclude Alport syndrome
idiopathic hypercalciuria
Idiopathic Hypercalciuria
  • RGH, persistent microscopic hematuria, or dysuria in the absence of stone formation
  • Hypercalciuria (without hypercalcemia)
  • Diagnosis: 24-hr urinary calcium excretion exceeding 4 mg/kg, urine calcium to creatinine ratio (mg/mg)
  • Hypercalciuria may lead to nephrolithiasis
  • RX: Oral thiazide
membranous glomerulopathy
Membranous Glomerulopathy
  • Uncommon in childhood and a rare cause of haematuria.
  • The most common cause of nephrotic syndrome in adults.
  • Associated with systemic lupus erythematosus, cancer, gold or penicillamine therapy, and syphilis and hepatitis B virus infections.
membranoproliferative mesangiocapillary glomerulonephritis
  • Chronic glomerulonephritis that frequently leads to glomerular destruction and end-stage renal failure.
  • Most common in the second decade of life.
  • Presentation: nephrotic syndrome, gross hematuria or asymptomatic microscopic hematuria, proteinuria and hypertension . renal function may be normal to depressed. Low C3 complement level.
  • Diagnosis by renal biopsy.
glomerulonephritis of chronic infection
  • Subacute bacterial endocarditis (S. viridans and other organisms)
  • Infected ventriculoatrial shunts for hydrocephalus (Staphylococcus epidermidis)
  • Syphilis, hepatitis B, hepatitis C, candidiasis, and malaria
  • Immune complexes, which deposit in the kidneys and initiate the glomerulonephritis.
  • The C3 level is frequently depressed.
rapidly progressive crescentic glomerulonephritis
  • Nephritis with rapid progression to end-stage renal failure
  • Causes: poststreptococcal, lupus, membranoproliferative, and the glomerulonephritides of Goodpasture disease, anaphylactoid purpura, and other forms of vasculitis
  • Acute renal failure, often after an acute nephritic or nephrotic episode
  • Diagnosis: Renal biopsy
  • Paediatric Nephrology Emergency
acute renal failure
Acute Renal Failure
  • Develops when renal function is diminished to the point at which body fluid homeostasis can no longer be maintained.
  • Oliguria (daily urine volume less than 400 ml/m2) is common, the urine volume may approximate normal.
  • Nonoliguric renal failure: in certain types of acute renal failure (aminoglycoside nephrotoxicity).
  • Prerenal causes
    • Hypovolemia, hypotension, hypoxia
  • Renal causes
    • Acute tubular necrosis
    • Acute interstitial nephritis
    • Glomerulonephritis
    • Localized intravascular coagulation
    • Tumors
    • Developmental abnormalities
    • Hereditary nephritis
  • Postrenal causes
    • Obstructive uropathy, stone, blood clot
clinical manifestations
  • Diminished urine output
  • Oedema (salt and water overload)
  • Hypertension, vomiting, and lethargy (uremic encephalopathy).
  • Complications of acute renal failure: volume overload with congestive heart failure and pulmonary edema, arrhythmias, gastrointestinal bleeding due to stress ulcers or gastritis, seizures, coma, and behavioral change
    • Life threatening: GIT bleed, pericarditis and encephalopathy
  • Careful history
  • Examination
  • Investigation: CBC, urea and electrolytes, PO4, Ca, blood gases, C3, US kidneys, urine electrolytes ( Na and creatinine), fractional excretion of Na (less than 1% in hypovalaemia)
urine analysis

Urine osmolality exceeds 500 mOsm/kg [mmol/l] H2O.

Sodium content is usually less than 20 mEq/l (mmol/l).

The fractional excretion of sodium (urine/plasma sodium concentration divided by the urine/plasma creatinine concentration X 100) is usually less than 1%.


osmolality less than 350 mOsm/kg [mmol/l] H2O

Usually exceeds 40 mEq/l (mmol/l)

Usually exceeds 1%

Urine Analysis
  • Pre-renal=Hypovolemia: volume replacement may be critical
  • Renal:
    • Fluid restriction: input= output + 400 ml/m2/24 hr (insensible losses)
    • Hyperkalemia: no potassium-containing fluid, foods, or medications until adequate renal function is re-established
      • > 7 mEq/L (mmol/L): Nebulised salbutamul, IV Calcium gluconate, sodium bicarbonate, ca resonium, glucose and insulin
    • Moderate acidosis is common in renal failure: Na bicarbonate
  • Hypocalcemia and hyperphosphataemia: Ca binders (Ca carbonate).
  • Hypertension:
    • The primary disease process (nifedipine, diazoxide, sodium nitroprusside or labetalol as a continuous intravenous infusion is indicated for hypertensive crises).
    • Expansion of the extracellular fluid volume (salt and water restriction is critical).
  • Indications for dialysis: fluid overload, and congestive heart failure, electrolyte abnormalities (especially hyperkalemia), central nervous system disturbances, hypertension.
  • In general, recovery of function is likely following renal failure resulting from prerenal causes, the hemolytic-uremic syndrome, acute tubular necrosis, acute interstitial nephritis, or uric acid nephropathy.
  • On the other hand, recovery of renal function is unusual when renal failure results from most types of rapidly progressive glomerulonephritis, bilateral renal vein thrombosis, or bilateral cortical necrosis.
chronic renal failure
Chronic Renal Failure
  • In children under 5 yr of age is commonly the result of anatomic abnormalities (hypoplasia, dysplasia, obstruction, malformations)
  • After 5 yr of age acquired glomerular diseases (glomerulonephritis, hemolytic-uremic syndrome) or hereditary disorders (Alport syndrome, cystic disease) predominate
  • UT malformation + Glomerulonephritis + Pyelonephritis….. > 50% of causes
clinical manifestations47
Clinical Manifestations
  • Nonspecific symptoms (headache, fatigue, lethargy, anorexia, vomiting, polydipsia, polyuria, growth failure).
  • Physical examination: pallor and weakness, hypertension, growth retardation and rickets.
  • Investigations:
    • CBC: anaemia.
    • Electrolytes: hyponatremia, hyperkalemia, acidosis.
    • BUN and creatinine (nitrogen accumulation and level of renal function).
    • hypocalcemia, hyperphosphatemia, osteodystrophy.
    • High of intact parathyroid hormone levels.
  • Diet in chronic renal failure.
  • Water and electrolyte management in chronic renal failure (fluid, K, Na).
  • Acidosis in chronic renal failure.
  • Renal Osteodystrophy.
  • Anemia in chronic renal failure.
  • Hypertension in chronic renal failure.
  • Drug dosage in chronic renal failure.
end stage renal failure
End-stage Renal Failure
  • Dialysis is generally initiated when the patient's GFR < 10 ml/1.73m2/minute
    • Continuous ambulatory peritoneal dialysis (CAPD)
    • Continuous cyclic peritoneal dialysis (CCPD)
    • Haemodialysis
    • Haemofiltration
  • Renal transplantation
thank you
Thank You

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