B/ 68 End stage kidney and renal failure Flashcards
Functions of the kidney
Excretion of waste products from the metabolism
Regulation of body salt and water balance
Maintenance of appropriate acid balance
Secretion of hormones and autacoids (local factors which behave as hormones)
Components of the kidney
Glomeruli, tubules, interstitium, blood vessels
General information about kidney disease and damage to components
Some disorders affect more than one structure. Damage to one of the components of the kidney can lead to secondary damage to another components or multiple other components.
Chronic disease eventually leads to damage to all the components of the kidney. This is what culminates into chronic kindey failure and what is called end stage kidney.
Two important terms regarding kidney damage
Azotemia and Uremia
Azotemia
A biochemical abnormality associated with renal failure. Characterized by blood urea nitrogen (BUN) being above 9mmol/L, and creatinin being above 120micromol/L.
Largely related to a decreased GFR. Azotemia can be divided into two forms: pre-renal azotemia and post-renal azotemia.
Pre-renal azotemia
Hypoperfusion of the kidney (such as in the case of shock) leads to a decreased GFR.
Post-renal azotemia
Due to obstruction of urine outflow below the level of the kidney.
Uremia
When azotemia progresses to include clinical manifestations and systemic biochemical abnormalities. Thus Uremia = azotemia + Clinical manifestations + biochemical abnormalities.
Clinical manifestations of uremia
Fluid electrolyte disturbances Calcium and phosphate disturbances Cardiac alterations Pulmonary alterations Haematopoietic alterations GI alterations Skin alterations Neuromuscular alterations
Fluid electrolyte disturbances
Tubular disease leads to polyuria. Polyuria can lead to dehydration and a high electrolyte level.
Glomerular problems can lead to decreased filtration which leads to salt and water retention. This can lead to edema, cardiac failure due to increased blood volume and hyperaldosteronism (which further increases the salt and water retention). Patients with kidney failure usually have metabolic acidosis because they have a decreased ability to remove waste products.
Calcium and phosphate disturbances
The kidney normally excretes phosphate. When the kidney is damaged, the concentration of phosphate increases. When phosphate increases, it binds calcium and decreases the concentration of calcium, which stimulates release of PTH. This all sums into renal osteodystrophy and hypermetastatitc calcifications.
Cardiac alterations
Uremia has toxic effects on the vessels which leads to increased permeability of the vessels - allowing for fibrinogen to leak out into the pericardium. This form the fibrous “bread and butter” pericarditis.
Left ventricular hypertrophy and cardiac failure occurs.
Pulmonary alterations
Pleuritis and hyaline membrane like disease as a consequence of the toxic effects (uremic pneumonitis).
Haematopoietic alterations
Anemia, because the synthesis of EPO is decreased. Increased bleeding tendency due to decreased production of tissue factor.
GI alterations
Gastroenteritis generated by the toxins.