52. Basic etiology and pathogenesis of renal disorders. Urinary syndrome, alterations in diuresis. Nephritic and nephrotic syndromes.

BASIC ETIOLOGY AND PATHOGENESIS OF RENAL DISORDERS. FUNCTIONAL SYNDROMES

Kidney functions

1. Production of urine
2. Regulation of RBC production
3. Regulation of blood pressure (renin)
4. Regulation of metabolic toxins and excess of water
5. Regulation of bloods acid-base balance
6. Regulation of mineral levels

Urine symptom into 2:

Quantitative

• 500 mL - 2 L average
• <500 - oliguria
• <100 - anuria
• >2000 mL - polyuria
• diuretics
• diabetes
• both

Qualitative

• Hematuria: caused by the glomerular filter
• true hematuria
• pseudohematuria
• rifampin
• excessive amount of beet, very like blood
• myoglobin, happens in cell damage
• bilirubin, beer-like urine
• Proteinuria: under 50 mg is okay but ideal should be very low.
• diabetes & hypertension
• amyloidosis of kidney
• glucosuria
• ketonuria
• bacteriuria
• lymphaturia

Renal disorders

• There are two main types of renal disorders

1. Glomerulopathies (glomerulonephritis)
2. Tubulo-interstitial disorders (pyelonephritis)

1) Glomerulopathies (glomerulonephritis)

• Glomerulonephritis - renal disease characterised by inflammation of the glomeruli, or small blood vessels in the kidneys (always involves both kidneys)
• The disease may occur as a:

1. Primary condition

• Usually result from an autoimmune conflict
• Glomerular disease is the only disease present

2. Secondary condition

• Glomerular abnormality results from another disease
• E.g. arterial hypertension, diabetes mellitus, SLE,

Pathogenesis of glomerulonephritis

• Two types of immune mechanisms have been implicated in the development of glomerular disease:

1. Auto-antibodies reacting with fixed glomerular antigens

• Antigens on basal membrane, podocytes
• After antigen binds to basal membrane → activates neutrophils, complement
• Antigens may have endogenous origin (DNA in SLE), or exogenous origin (streptococcal membrane antigens in poststreptococcal glomerulonephritis)

2. Circulating antigen-antibody complexes that become trapped/deposited in the glomerular membrane

• Hypersensitivity type III reaction
• Occurs in SLE
• Accumulate in glomerular capillaries → inflammatory reaction
• Good pasture syndrome - glomerulonephritis, with or without pulmonary hemorrhage, and the presence of circulating anti-glomerular basement membrane (anti-GBM) antibodies
• Binding of auto-antibodies activates complement
• Type II antigen-antibody reaction
• The cellular changes that occur with glomerular disease are:

1. Proliferative - an increase in the cellular components of the glomerulus
2. Sclerotic - an increase in the noncellular components of the glomerulus, primarily collagen
3. Membranous - an increase in the thickness of the glomerular capillary wall, often caused by immune complex deposition

Signs and symptoms of glomerulonephritis

• Signs of glomerular damage are:
• Increased permeability of the basal membrane
• Decreased overall GFR
• Dysfunction of jugular-glomerular apparatus
• Glomerular-tubular disbalance

Acute glomerulonephritis

• Most causes are infectious → follows a streptococcal infection
• Is also related to systemic disease (SLE)
• Manifestations:

1. Macrohematuria - dark brown or smoky urine
2. Edema - starts in the eyelids and face → lower and upper limbs → generalised