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Module 7: Urogenital > Kidney pathology (7.5) > Flashcards

Kidney pathology (7.5) Flashcards

1
Q

Describe the classification of renal disease using clinical and morphological descriptions

A

Morphological: Vascular, glomeruli, tubular/interstitial

  • Compromise/damage in one morphological component will lead to damage in another (e.g. vascular compromise will lead to iscahemia of the tubules)

Clinical:

Total: Acute and chronic renal failure

Partial (may all lead to chronic renal failure): nephrotic syndrome, nephritic syndrome, haematuria and perisistant proteinuria

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2
Q

Compare and contrast acute and chronic kidney failure

KEY WORDS

A

Extra notes below - see table:

  • Acute kidney disease: Nitrogenous waste products (e.g. urea) accumulate within the blood, as filtration via the nephrons is lost
  • CKD: Irreversible, gradual loss which is normally due to long term conditions e.g. hypertension and diabetes. Initially asymptomatic
  • Chronic kidney disease: Determined by GFR. ↓ GFR leads to ↑ nitrogenous waste (demonstrated as risin creatinine levels)
  • Effects of chronic kidney disease:

THINK OF THE FUNCTIONS OF THE KIDNEY → NOW LOST

Increased Na+ and H2O levels; hyperkalaemia; uremia; ↓ EPO production; acidosis; decreased vitamin D activation → HPT

  • Bone disease in chronic kidney disease: PTH is released in response to decreased serum [Ca2+]. Renal vitamin D synthesis creates negative feedback, decreasing PTH secretion which in turn decreases the reabsorption of calcium from bone.
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3
Q

Acute renal failure: Outline acute tubular necrosis

A

☆Most common cause of acute renal failure☆

Necrosis of PCT and DCT epithelium resultant of ischaemia or toxic damage within the region.

The PCT and DCT epithelium have a high metabolic demand (active processes for ion transport etc).

Ischaemia or toxic damage causes cell death. The cells are shed and block the tubules - causing oligouria, uraemia and fluid overload. This oliguric phase creates a risk of acute renal failure.

CASTS (cell debris) observed in the urine.

In recovery polyuria is seen as the necrotic cells undergo phagocytsis and the tubule is again patent. The epithelium is not yet mature enough to be functional, causing increased urine output (polyuria). Fluids and electrolytes must be replaced to prevent imbalace and infection.

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4
Q

Describe the pathogenesis of diseases affecting the kidney tubules and interstitium - tubulointersititial disease

A

Tubuloinsterstitial disease: Affecting the tubules (DCT and PCT - due to high metabolic demand) and interstitium

Commonly caused by:

  • Infection (bacterial → pyelonephritis)
  • Ischaemia
  • Toxic damage e.g medications
  • Ischamia and toxic damage ⇒ acute tubular necrosis (ATN)
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5
Q

Describe factors contribuing to vascular disease of the kidney

A
  • Hypertension: Causes ateriolosclerososis leading to ischaemia
    • Reduced renal perfusion → activation of RAAS → hypertension → arteriolosclerosis of renal arteries → ischaemia in nephrons. If many damaged → chronic renal failure

Precipitates HT through RAAS but then is damaged by the hypertension created!

  • Diabetes
  • Renal artery stenosis via atherosclerosis (causes hypertension via RAAS activation, as kidney perfusion is decreased)
  • Embolic occlusion and infarction
  • Hypotension: May cause acute tubular necrosis (via poor perfusion)
  • Microthrombosis
  • Medications: Those which reduce renal blood flow e.g. NSAIDS, ACEi, diuretics
  • RAAS activation → hypertension → renal damage
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6
Q

Describe the effects of diabetes on the kidney

A

Vascular:

  • Increased susceptibilty to atheroma. Hyaline arteriolosclerosis may ensue. This is turn may cause poor glomerular perfusion. Ischaemia of the glomerulus and tubules results, leading to nephron death. Chronic kidney failure follows

Glomerular:

  • Basement membrane becomes thickened and leaky (glomerular hyalinisation). Proteinuria/microalbuminuria results, creating nephrotic syndrome and ultimately chronic kidney failure.
  • Mesangial sclerosis causing the mesangial cells to crush the poorly perfused glomerular capillaries

Tubules & interstitium:

  • Diabetes creates increased susceptibilty to infection
  • The tubules may undergo atrophy due to vascular/glomerular disease → chronic renal failure
  • Acute pyelonephritis sees the collection of pus in the tubules and collecting ducts → acute renal failure
  • A combination of the above leads to renal papillary failure (papillary necrosis due to vasa recta inflammation) → acute renal failure
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7
Q

Describe how renal disease may cause secondary hypertension (HT)

Acute/chronic kidney disorders, reno-vascular disease

A

Acute kidney disorders

  • Can cause at least temporary hypertension
  • Hypertension results from decreased urine formation and increased sodium and water retention

Chronic kidney disorders

  • Hypertension is common

Reno-vascular disease: Renal stenosis

  • Atherosclerotic disease of renal blood vessels → reduced renal blood flow → RAAS is activated → vasoconstriction → sodium and water retention → hypertension
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8
Q

Describe the normal glomerular structure and its possible responses to injury

A

Normal structure: Glomerular capillary epithelium, glomerular basement membrane, podocytes

Damage via vascular disease, immunological disorders, deposition of foreign material (amyloid)

Responses to injury:

  • Endothelial cell proliferation (→ decreased flow and oliguria)
  • Mesangial and/or matrix proliferation
  • Glomerular basement membrane thickening
  • Changes in podocyte processes
  • Capillary necrosis (fibrinoid)
  • Fibocellular crescent formation
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9
Q

Describe the role of immune damage in glomerular disease

A
  1. Deposition of circulating immune complexes at the basement membrane or megangium: Common
  2. Circulating antigen entrapment leading to Ig binding: Cause of lupus
  3. Anti-GBM Igs: The autoantibodies cause damage to a GBM component (alpha 3 domain). Seen in the rare Goodpasture’s syndrome
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10
Q

Describe patterns of glomerula disease

(‘distribution’ of disease)

A

Focal: Affects some glomeruli

Segmental: Affecting one area of a single glomerulus

Diffuse: Affecting all the glomeruli

Global: Affecting the whole of a glomerulus

e.g. focal segmental

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11
Q

Compare and contrast the morphological features and clinical manifestations of the nephrotic and nephritic syndromes

A
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12
Q

Describe the clinical classification of glomerular disease

A

Acute nephritic syndrome

Rapidly progressive glomerulo-nephritis

Nephrotic syndrome

Asymptomatic haematuria or proteinuria

Chronic glomerulonephritis

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13
Q

Describe an example of a glomerular disease in each clinical category

A
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14
Q

Describe the clinical classification and manifestations of glomerular disease including the nephrotic and nephritic syndromes

Nephritic syndrome: Description, pathophysiology, clinical manifestations, examples

A

Description: Proliferative, inflammatory.

Pathophysiology: Acute inflammation of the glomerulus

  • Causes damage to capillary walls → red cell casts in urine
  • Occlusion of the capillary lumen (due to the proliferation of cells and influx of inflammatory cells)

Clinical manifestations:

  • Haematuria
  • Decreased GFR → causing hypertension and oedema
  • Oliguria, azotemia

Examples:

  • Acute post-infectious glomerulonephritis
  • SLE
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15
Q

Nephritic syndromes

Acute postinfectios GN (glomerulonephritis): Description, pathophysiology, aetiology, clinical manifestations, treatment

A

Description: Diffuse

Pathophysiology:

  • As endothelial and mesangial cells swell and proliferate the lumen becomes occluded
  • Neutrophils and monocytes infiltrate
  • Immune complexes develop following infection (see aetiology) and are deposited in the mesangium and basement membrane

Aetiology:

  • Post-strep throat infection
  • Viral
  • Staph.

Clinical manifestations:

  • Haematuria (cola coloured)
  • Mild hypertension
  • Oliguria
  • Proteinuria

Treatment:

  • Antibiotics
  • Mostly seen in children - has good prognosis
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16
Q

Describe the clinical classification and manifestations of glomerular disease including the nephrotic and nephritic syndromes

Assymptomatic haematuria and proteinuria: Description, progression, examples

A

Description: A nephritic condition. Mild proteinuria, haematuria or reduction in GFR

Progression: Can progress to chronic kidney disease over years

Examples:

  • Alport syndrome: X-linked hereditary defect in GBM type IV collagen. Effects also seen in cornea and cochlea.

Presents as haematuria at 5 -20 years and then may progress to kidney failure.

17
Q

Describe the clinical classification and manifestations of glomerular disease including the nephrotic and nephritic syndromes

Assymptomatic haematuria and proteinuria (Berger disease): Description, pathophysiology, clinical manifestations

A

Description: IgA nephropathy - Berger disease. Most common cause of nephritic syndrome

Pathophysiology: IgA immune complexes accumulate in the mesangium. Proliferation of mesangial cells

Clinical manifestations:

  • Haematuria and loin pain in young adults/children - following resp. tract infection
  • Reoccurs and can lead to chronic renal failure
18
Q

Describe the clinical classification and manifestations of glomerular disease including the nephrotic and nephritic syndromes

Rapidly progression glomerulonephritis: Description, pathophysiology, clinical manifestations, examples

A

Description: Clinical syndrome resultant of immune complex deposition or anti-GBM antibodies

Pathophysiology:

  • Immune complex or anti-GBM antibodies
  • Anti-GBM Igs may also affect the lung
  • Crescents may be seen: Formed by proliferation of parietal epithelium of Bowman’s capsule and influx of inflammatory cells

Clinical manifestations:

  • Nephritic syndrome
  • Oliguria
  • Rapid renal failure

Examples:

  • Goodpasture’s syndrome
19
Q

Describe the clinical classification and manifestations of glomerular disease including the nephrotic and nephritic syndromes

Nephrotic syndrome: Description, clinical manifestations

A

Description: Increase in glomerular permeabilty and consequent loss of plasma proteins (mainly albumin) in the urine

Clinical manifestations:

  • Proteinuria ( > 3.5 mg/day)
  • Hypoalbuminaemia
  • Generalised oedema (due to reduced oncotic pressure)
  • Hyperlipidaemia and lipiduria (as no lipoproteins for binding)
20
Q

Outline the consequences of protein loss

A
  • Oedema: Reduction in colloid osmotic pressure, allowing for fluid accumulation. Blood volume decreases → RAAS and SNS activation. Reduced natriuretic factors.
  • Dyspnoea: Due to pleural oedema
  • Increased infection: Loss of Igs and complement in urine
  • Increased atherosclerosis: Due to hyperlipidaemia
  • Low levels of hormones and ions: Due to decreased binding proteins
  • Thromboembolic events: Due to loss of balance between coagulation and anti-coagulation factors
21
Q

Describe the clinical classification and manifestations of glomerular disease including the nephrotic and nephritic syndromes

Minimal change disease: Description, pathophysiology

A

Description: Diffuse. Does not progress to renal failure. Presents in children.

Pathophysiology: Podocyte effacement. Allows release of protein

22
Q

Describe the clinical classification and manifestations of glomerular disease including the nephrotic and nephritic syndromes

Focal segmental glomerulosclerosis: Description, pathophysiology, aetiology

A

Description: Focal and segmental = only seen in some parts of the glomeruli.

Pathophysiology:

  • Sclerosis = increased collagen deposition in the mesangial matrix

Aetiology:

  • Idiopathic
  • Associated with heroin use
  • HIV infection
  • Sickel cell or other diseases causing reduced oxygen in the blood
  • Can be a progression of IgA nephropathy
23
Q

Describe the clinical classification and manifestations of glomerular disease including the nephrotic and nephritic syndromes

Membranous glomerulonephrtis: Description, pathophysiology

A

Description: Diffuse, global GBM thickening

  • Mostly idiopathic

Pathophysiology:

  • Igs react to pathogens trapped within the glomerulus BUT no inflammatory or proliferative response
  • Subepithelial immune complex deposits
  • Podocyte effacement
24
Q

Describe the clinical classification and manifestations of glomerular disease including the nephrotic and nephritic syndromes

Membranoproliferative glomerulonephritis: Description, pathophysiology

A

Description: Diffuse global GBM thickening

  • Presents in young adults. Poor prognosis

Pathophysiology:

  • Subendothelial immune complex deposits
  • Proliferation of mesangial cells (mixed nephrotic/nephritic)
25
Q

Describe the clinical classification and manifestations of glomerular disease including the nephrotic and nephritic syndromes

Chronic glomerulonephritis: Findings, progression, treatment

A

Due to the high functional reserve of the kidney chronic GN is often an incidental finding.

Progression:

  • Sclerosis of glomeruli
  • Reduction in proteinuria as the glomeruli fail

Treatment:

  • Dialysis
  • Transplantation
26
Q

Outline nephrotic and nephritic syndromes

Description and consequences

A

Nephrotic = Severe damage to the GBM and mesangium → increased permeabilty and leakiness

Nephritic = Proliferation of mesangium and endothelium of glomerulus → occlusion of glomerular capillaries

27
Q

Suggest possible pre-renal, renal and post-renal causes of acute kidney disease

A

Unilateral obstruction can be silent for a long period due to compensation from the opposite kidney.

28
Q

Acute renal failure: Nephrotoxic drugs

  • How may they cause renal damage/injury?*
  • Key examples of nephrotoxic drugs*
A
  • Direct action on cells
  • Obstruction of tubules via crystal formation (sulfonamides)
  • Producing hypersensitivity type reactions leading to tubule and interstitial damage
  • Through reducing blood flow e.g. NSAIDS, diuetics

Key examples:

NSAIDS, diuretics, aminoglycosides (gentamycin), ACEi, ARBs

☆ Be especially aware of drugs that alter haemodynamics - can causes changes in renal perfusion and GFR

Module 7: Urogenital (29 decks)

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