Chronic kidney disease Flashcards
Define chronic kidney disease
Term used to describe deteriorating kidney function of any underlying cause. It is long standing (>3 months), progressive and shows impairment in renal function.
State different causes of chronic kidney disease
Outline the stages of chronic kidney disease
Pathophysiology changes in chronic kidney disease.
Regardless of the method of renal injury (i.e., diabetes, hypertension, or glomerular disorders), once renal damage has occurred, a cascade of events ensues.[15][16]
In response to renal injury, there is thought to be an increase in intra-glomerular pressure with glomerular hypertrophy, as the kidney attempts to adapt to nephron loss to maintain constant glomerular filtration.
An increase in glomerular permeability to macro-molecules such as transforming growth factor-beta (TGF-beta), fatty acids, pro-inflammatory markers of oxidant stress, and protein may result in toxicity to the mesangial matrix, causing mesangial cell expansion, inflammation, fibrosis, and glomerular scarring.
Additionally, renal injury results in an increase in angiotensin II production, causing an upregulation of TGF-beta, contributing to collagen synthesis and renal scarring within the glomerulus.
Both the structural alterations and accompanying biochemical, cellular, and molecular changes seem to account for progressive renal scarring and loss of kidney function.
All forms of CKD are also associated with tubulo-interstitial disease; the exact mechanism of injury is not known, but is thought to be secondary to a reduction in blood supply in addition to an infiltration of lymphocytes and inflammatory mediators that result in interstitial fibrosis and tubular atrophy.
State potential compliciations of CKD
- Anaemia
- erythropoeitin deficiecny
- Increased red cell destruction in uraemia
- haemodialysis can also cause red cell destruction
- toxins to bone marrow (these are retained in CKD)
- Increased bleeding time - platlet function is impaired in CKD
- Mineral and bone disorders
- changes in calcium, phosphorys, PTH and vitamin D metabolism
- impaired conversion to active vitamin D - which results in reduced absorption of calcium in intestines - causes osteoclastic bone resorption - also releasing phosphate
- changes in calcium, phosphorys, PTH and vitamin D metabolism
- CVD
- increased risk in CKD patients
- various factors from CKD contribute
- Hypertension
- Diabetes mellitus (the most common cause of CKD)
- Smoking
- Male gender
- Mechanisms
- increased calcium causes calficiation of vessels - increasing pulse pressure
- Endorcrine disease
- Half life of insulin is increased to decreaasted tubular metabolism - potentially leading to diabetes
- Fluid electrolyte imbalance
- Metabolic acidosis
- Fluid retention
The aims of management of chronic kidney disease are to reduce progression of the disease.
Monitoring of renal function
The rate of change in renal function varies between patients and may vary over time in each individual. Renal function should therefore be monitored every 6 months in patients with stage 3 CKD, but more frequently in patients who are deteriorating rapidly or have stage 4 or 5 CKD
Antihypertensive therapy
Lowering of blood pressure slows the rate at which renal function declines in CKD
Reduction of proteinuria
Patients with proteinuria are at higher risk of progression of renal disease, and there is strong evidence that reducing proteinuria reduces the risk of progression. ACE inhibitors and ARBs reduce proteinuria and retard the progression of CKD, While ACE inhibitors and ARBs are excellent drugs for patients with diabetes or CKD and proteinuria, they need to be prescribed with care in certain circumstances. Initiation of treatment with ACE inhibitors and ARBs may be accompanied by an immediate reduction in GFR; patients should therefore have their renal function checked within 7–10 days of initiating or increasing the dose of an ACE inhibitor or ARB. Treatment can be continued so long as the reduction in GFR is not greater than 25% and is not progressive
treatment of anemia - recombinant human EPO
treatment of electrolyte imbalance - reduced protein intake, reduce potassium intake, sodium reductiuon (diuretics often required)
treatment of acid-base disorders - Reduced ability to excrete organic acids in patients with CKD may lead to an anion-gap metabolic acidosis. In addition, in patients with tubulo-interstitial disease or diabetic nephropathy, there may be specific defects in acid–base regulation within the kidney, causing a non-anion-gap renal tubular acidosis (p. 365). Although acidosis is usually asymptomatic, it may be associated with increased tissue catabolism and decreased protein synthesis, and may exacerbate bone disease and the rate of decline in renal function. Hence, plasma bicarbonate concentrations should be maintained above 22 mmol/L by prescribing sodium bicarbonate supplements (starting dose of 1 g 8-hourly, increasing as required). There is some evidence that correcting acidosis may reduce the rate of decline in renal function.
treatment of renal bone disease - gut phosphaye binders, nicotinamide. Calcitriol analogues, Cinacalcet (acts on parathyroid sensing hormone receptor - leading to parathyroid to respond as though serum calcium levels were high - thereby reducing PTH synthesis and release./
Outline investigations for CKD
What is renal replacement therapy? How is it used?
- Essentially replacing the kidneys function with haemodialysis or peritoneal dialysis
- It eliminates wastes, mimics electrolyte concentrations, prevents acid/base imbalance, maintains extracellular volume.
What are the main 4 options for renal replacement therapy?
A In haemodialysis, there is diffusion of solutes from blood to dialysate across a semipermeable membrane down a concentration gradient. B In haemofiltration, both water and solutes are filtered across a porous semipermeable membrane by a pressure gradient. Replacement fluid is added to the filtered blood before it is returned to the patient. C In peritoneal dialysis (PD), fluid is introduced into the abdominal cavity using a catheter. Solutes diffuse from blood across the peritoneal membrane to PD fluid down a concentration gradient, and water diffuses through osmosis (see text for details). D In transplantation, the blood supply of the transplanted kidney is generally anastomosed to the external iliac vessels and the ureter to the bladder. The transplanted kidney replaces all functions of the failed kidney.
