Chrissa Mae T.

Catindoy BS Medical Technology 3A

FINALS [LECTURE I]: AUBF: Renal disease

Classification:

• Glomerular disorders
• Tubular disorders
• Interstitial disorders
• Renal lithiasis

Glomerular disorders

- Majority are of immune origin.

o Immune complexes from immunologic disorders throughout the body.
o Increased serum IgA.
o Immune system mediators – complement.
- Nonimmunologic.
o Chemicals and toxins
o Deposition of amyloid material and acute phase reactants
o Electrical charge interference
o Membrane thickening

Glomerulonephritis

- General term for sterile, inflammatory process affecting the glomerulus.

- Causes blood, protein, and casts in urine.

**NOTE: Types of glomerulonephritis progress through various disorders:

Acute glomerulonephritis → Chronic glomerulonephritis → Nephrotic syndrome → Renal failure

Acute Post-streptococcal Glomerulonephritis (AGN)

- Group A streptococcal infections from organisms with M

protein in the cell wall.
o Fever
o Edema (around eyes)
o Oliguria
o Hematuria
o Proteinuria
- Immune complexes deposit on glomerular membranes.
- Can be seen:
o RBC casts o Granular casts
o Dysmorphic RBCs o WBCs
o Hyaline cast
- Anti–group A streptococcal enzyme tests.

Rapidly Progressive (Crescentic) Glomerulonephritis

- More serious acute form → renal failure.

- Systemic immune disorders:
o Macrophages damage capillary walls.
o Fibrin = permanent damage to capillary tufts.

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- Urinalysis similar to AGN progresses to more abnormal, high-protein, low glomerular filtration
rate (GFR).
- May have (+) fibrin degradation products and cryoglobulins.

Goodpasture’s syndrome

- Autoimmune disorder against glomerular and alveolar

basement membranes.
- Cytotoxic Ab following viral respiratory diseases: anti-
glomerular basement membrane Ab
o Hemoptysis
o Hematuria
o Proteinuria
o RBC casts
- Chronic glomerulonephritis to end-stage renal failure.

Wegener’s granulomatosis

- Inflammation and granulomas in small blood vessels of

lungs and kidney.
- Anti-neutrophilic cytoplasmic Ab.
- Neutrophils initiate immune response, producing
granulomas.
o Pulmonary symptoms (first)
o Hematuria
o Proteinuria
o RBC casts
o Elevated serum BUN and creatinine levels

Henoch-Schönlein purpura

- Children following respiratory infections.

- Raised, red patches on skin.
- Blood in sputum and possibly stools.
o Proteinuria
o Hematuria
o RBC casts
- 50% complete recovery.
- Follow patients for more serious renal problems.

Membranous glomerulonephritis

- IgG immune complexes on glomerular basement

membrane cause thickening.
- These aid in diagnosis:
o Systemic lupus erythematosus
o Sjögren’s syndrome
o Secondary syphilis
o Hepatitis B
o Gold and mercury treatments
o Malignancy and Thrombosis

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- Slow progression, remission, nephrotic syndrome.
o Microscopic hematuria
o very high protein

Membranoproliferative glomerulonephritis

- Type 1: thickening of capillary walls; progresses to

nephrotic syndrome.
- Type 2: glomerular basement membrane thickening
progresses to chronic glomerulonephritis.
o Hematuria
o Proteinuria
o ↓ complement
- Autoimmune disorders, infections, malignancies.

Chronic glomerulonephritis

- Progression from previous disorders.

o Hematuria
o Proteinuria
o Glycosuria (tubular damage)
o Broad cast
o Waxy cast
- Gradually worsening:
o Fatigue o Edema
o Anemia o Oliguria
o Hypertension
- Markedly decreased GFR
- Increased BUN and creatinine and electrolyte imbalance.

Berger’s disease

- “Immunoglobulin A nephropathy”
- Most common cause of glomerulonephritis.
- IgA complexes on glomerular membrane.
- Increase serum IgA.
- Early macroscopic hematuria from exercise or infection with spontaneous recovery.
- 20 years later: gradual progression to chronic glomerulonephritis.
- Granular and disintegrating RBC casts.

Nephrotic syndrome

- Acute onset from systemic shock (low blood pressure) or

glomerulonephritis complication.
- Glomerular membrane damage and changes in podocyte
electrical charges.
- Protein passes through membrane; serum albumin depleted,
causing increased lipid production.
- Edema from loss of oncotic pressure.
- Tubular damage.
- Marked proteinuria >3.5 g/day

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o Fat droplets o Waxy casts
o Oval fat bodies o Microscopic hematuria
o Fatty casts
o Renal tubular epithelial cells and casts

Lipid Nephrosis

- “Minimal change disease”

- Children, allergic reactions, immunization, HLA-B12.
o Heavy proteinuria
o Edema
o Transient hematuria
- Normal BUN and creatinine levels.
- Good prognosis, steroids, remission.

Focal segmental glomerulonephritis

- Similar to nephrotic syndrome but affects only certain

numbers and areas of glomeruli; podocytes are damaged.
- IgM and C3 immune deposits.
o Moderate to heavy proteinuria
o Microscopic hematuria
- Heroin and analgesic abuse, HIV.

Alport’s syndrome

- Inherited sex-linked and autosomal disorder affecting

basement membrane.
- Males more severely affected.
o Macroscopic hematuria
o Respiratory infections (age 6 years)
- Membrane laminated with thinning.
- No immune complexes.
o Mild to persistent hematuria
- Later nephrotic syndrome, renal failure for some.

Kimmelstiel-Wilson disease

- “Diabetic nephropathy”
- Most common cause of end-stage renal disease.
- Glomerular basement membrane thickening.
- Increased proliferation of mesangial cells.
- Increased deposition of cellular and acellular material within
matrix of Bowman’s capsule and around capillary tufts.
- Deposition associated with glycosylated proteins from poorly
controlled diet.
- Sclerosis of vascular structure.
- Reason for early microalbumin testing.

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Tubular disorders

Acute tubular necrosis

- Ischemia: severe decrease in blood flow (Shock).

o Trauma
o Surgery
o Cardiac failure
o Electricity
o Toxigenic bacteria
o Anaphylaxis
o Massive hemorrhage
- Nephrotoxic agents:
o Aminoglycosides o Heavy metals
o Amphotericin B o Mushroom poisoning
o Radiographic dye o Hemoglobin
o Ethylene glycol o Myoglobin
- Remove cause and manage symptoms.
- Noticeable renal tubular epithelial (RTE) cells and casts and RTE fragments.
o Hyaline
o Waxy cast
o Granular
o Broad casts

Fanconi syndrome

- Proximal convoluted tubule reabsorption failure.

- Inherited with cystinosis and Hartnup disease.
- Acquired: heavy metals, outdated tetracycline.
- Complication of multiple myeloma, renal transplant.
- Glycosuria and electrolyte imbalance.
- Mild proteinuria.

Nephrogenic diabetic insipidus

- 2 types:
o Nephrogenic: failure of tubules to respond to:
▪ Antidiuretic hormone (ADH)
▪ Inherited sex-linked recessive
▪ Lithium and amphotericin B exposure
▪ Polycystic kidneys
▪ Sickle cell anemia
o Neurogenic: failure to produce ADH
- Urine: pale yellow, low specific gravity (SG), possible negative results for other tests.

Renal Glycosuria

- Affects only the reabsorption of glucose.

- Inherited as autosomal recessive.
- Decreased number of glucose transporters in tubules.
- Decreased affinity of transporters for glucose.

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- Glyucosuria with normal blood glucose level.

Interstitial disorders

Tubulointerstitial Diseases

- Infections and inflammations affecting the interstitium and

the tubules.
- Most common renal disease is urinary tract infection (UTI).
- Cystitis (bladder infection) is very common.
- Symptoms: urinary frequency and burning.
- Untreated: progresses to upper urinary tract.
- Presence of:
o WBCs o Mild proteinuria
o Bacteria o Hematuria
o Increased pH
**NOTE: WBCs in urine called pyuria.

Acute Pyelonephritis

- Ascending movement of bacteria.

o Conditions affecting emptying of bladder.
o Calculi
o Pregnancy
o Reflux of urine from bladder to ureters
- Symptoms:
o Rapid onset
o Lower back pain
o Urinary frequency
o Burning
- Urinalysis: similar to cystitis with 1 exception – presence of WBC casts.

Chronic Pyelonephritis

- Damage to tubules, possible renal failure.

- Congenital structural defects causing reflux are most common
cause.
- Can affect emptying of collecting ducts.
- Often diagnosed in children.
- Early urinalysis similar to acute pyelonephritis.
- Presence of:
o Later granular
o Waxy cast
o Broad casts
- Increased protein, hematuria
- Decreased SG.

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Acute Interstitial Nephritis

- Allergic reaction causing inflammation of interstitium and

tubules.
- Medication allergy to:
o Penicillin
o Methicillin
o Ampicillin
o thiazide diuretics
o Cephalosporins
o NSAIDs
**NOTE: If discontinue use steroids.

- Urinalysis:
o Hematuria o ↑ WBCs
o Proteinuria o WBC casts

**NOTE: No bacteria.

- Hansel stain for eosinophils.

Renal Failure

- Acute and chronic forms.

- Chronic renal failure.
o Progression from original disorders to end-stage
renal disease.
o GFR <25 mL/min
▪ ↑ BUN and creatinine levels
▪ Electrolyte imbalance
▪ Isosthenuria
▪ Proteinuria
▪ Renal glycosuria
- Lack of renal concentrating ability.
- Presence:
o ↑ granular o Broad casts
o Waxy casts
Acute Renal Failure

- Sudden onset, often reversible.

o Prerenal: Decreased blood flow
o Renal: acute disease
o Postrenal: renal calculi and tumors
- Urinalysis:
o RTE cells – decreased blood flow
o RBCs – glomerular damage
o WBCs and WBCs casts – infection/inflammation
o Urothelial cells – possible bladder tumor
- Symptoms:
o Decreased GFR o Edema
o Oliguria o Azotemia

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Chrissa Mae T. Catindoy BS Medical Technology 3A
- Causes:
o Prerenal
▪ Hemorrhage ▪ Surgery
▪ Burns ▪ Septicemia
▪ ↓ blood pressure/cardiac output
o Renal
▪ Acute glomerulonephritis
▪ Acute tubular necrosis
▪ Acute pyelonephritis
▪ Acute interstitial nephritis
o Postrenal
▪ Renal calculi
▪ Tumors
▪ Crystallization of ingested substances

Renal lithiasis

- Renal calculi (kidney stones) in calyces and pelvis of

kidney, ureters, bladder.
- Staghorn, round and smooth, barely seen.
- Severe back pain radiating from lower back to legs when
passing.
- Lithotripsy: high energy shock waves break up stones.

**NOTE: Also, surgical removal.

- Formation conditions similar to crystals.

o pH o Stasis
o Concentration
o No exact cause of formation known
o Increased in the summer (dehydration)
- Types of stones:
o 75% calcium oxalate or phosphate.
o Magnesium ammonium phosphate (struvite).
▪ UTI and ↑ pH, like triple phosphate crystals
o Uric acid: increased purine diet
o Cystine: hereditary cystinosis

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This property is governed by Republic Act No. 386, Title II, Chapter 1, Article 429 of Property Law of the Philippines.