L29 Chronic Kidney Disease Flashcards
What is filtered from the blood at the Proximal convoluted tubule?
1) Reabsorbs 65% of filtrate volume: nutrients (glucose, amino acids)/ ions(Na/bicarb)/ water
2) Secretes toxins (ammonium, creatinine, organic acids, some drugs)
3) Adjusts filtrate pH
What is filtered from the blood at the Descending limb of the loop of Henle?
Water reabsorption (aquaporins) = increased osmolality
The fluid entering the descending limb contains sodium chloride and other salts, urea and other chemicals that have been filtered out from the blood. The cells here are permeable to water and thus the salt and urea concentration rises within the fluid by the time it reaches the bend.
What is filtered from the blood at the ascending limb of the loop of Henle?
Reabsorbs Na/Cl = reduces osmolality Urea secreted (urea recycling)
The thick ascending limb expresses a sodium-potassium-chloride cotransporter and helps reabsorb approximately a third of the filtered sodium and chloride from the fluid in the tubular lumen into the blood
What is filtered from the blood at the distal convoluted tubule?
Aldosterone acts here leading to the reabsorption of Na (Cl follows), secrete K.
PTH acts here leading to reabsorption of Ca.
Reabsorption of bicarb and water and synthesises bicarbonate.
What is CKD?
Chronic Kidney Disease: A diagnosis requires abnormality in the structure or kidney, present at least 2 occasions, 3 months apart. There are 5 stages of CKD - this is determined using eGFR.
In what populations is CKD more prevalent?
Prevalence rises with age. More common in south Asians (due to higher prevalence with diabetes) and black people (due to the higher chance of HTN) and genetic causes.
What is ACR?
Urine albumin to creatinine ratio (ACR), also known as urine microalbumin, helps identify kidney disease.
What are the causes of CKD?
Causes (there are many): - Diabetes is the most common - HTN (also very common) - Glomerular disease, e.g. chronic GN, lupus nephritis - Vascular disease, e.g. RAS - Infections - Urinary tract obstruction or dysfunction, e.g. stones - Cystic kidney diseases - Inherited disorders, e.g. Alport syndrome - Tubulointerstitial disease - Multiple Myeloma - AKI - Trauma Unknown
What is the aetiology of CKD?
There is raised intraglomerular pressure. This damages nephrons. The remaining nephrons try and compensate. They will filter through the remaining glomeruli faster - to try and compensate - this is known as hyperfiltration. Hyperfiltration to the glomeruli causes damage to the glomeruli. This may mean that more protein is lost, and so as CKD progresses, more protein is found in the urine. Following this adaption there is:
- hyperfiltration
- Increased Permeability of the glomerular leads to glomerular sclerosis - expansion of the glomerular mesangium (the space continuous with the smooth muscle of the arterioles - it is outside the lumen by surrounded by capillaries) and deposition of the extracellular matrix
- Tubulointerstitial fibrosis - some of the tubules will atrophy, this means interstitial inflammatory cells infiltrate, leading to deposition of EC in the interstitial
- Loss of the renal cortex
- Shrunken kidney (irreversible)
How is CKD diagnosed?
Diagnosis
- The eGFR
- Urine-albumin creatine ratio
Blood pressure (test for those at risk)
What is the clinical presentation of CKD?
Patients are often asymptomatic from stages 1-3. Later on they will develop symptoms, they are quite non-specific as to what they will develop. Clinical manifestations include:
- Lethargy, reduced exercise tolerance, shortness of breath and impaired immune function due to anaemia
- They may have signs of the underlying disease such as LUPUS, they may start showing signs of lupus
- Often a lack of appetite
- Metabolic taste in the mouth
- Weight loss
- Vomiting
- Due to impaired salt and water balance, they will develop peripheral oedema, pedal odema (fluid accumulation in the feet and lower legs) and reduced urine output
- Aches and pains in the joints due to impaired activation of vitamin D and therefore calcium absorption
As CKD progresses towards stage 5 CKD, they may develop uraemia.
What is uraemia?
High levels of urea in the blood. This can lead to uraemic pericarditis, encephalopathy, and ureamic frost (urea and urate deposit on skin). Pericarditis can lead to cardiac tamponade. Encephalopathy may lead to seizures, coma, confusion and impaired function.
What are the complications of uraemia?
Can progress to end stage renal failure. Stage 4 or 5 CKD tend to progress to end stage renal failure. CKD has implications of the heart - increased risk of heart failure, heart attack. They are more at risk of developing AKI, frailty and mortality. CKD may lead to menstrual irregularities (or amenorrhea); may also lead to greater deterioration when pregnant.
What further investigations are used in the diagnosis of CKD?
Target investigations looking at underlying cause - bloods, immunology screen, imaging for signs of obstruction and renal biopsy to see abnormalities on histopathology.
What factors influence CKD progression?
Non-modifiable:
- Underlying cause of kidney disease
- Race
Modifiable:
- Blood pressure - lifestyle changes, optimising BMI, low salt diet, exercise, ACEi/ARB (also reduce the amount of protein excreted)
- Level of proteinuria
- Dyslipidaemia - consider a statin
- Underlying disease activity
- Further renal insults (superimposed obstruction, UTI)
- Hypovolaemia/intercurrent illness - decrease in volume
- Exposure to nephrotoxic agents
- Hyperphosphatemia
- Metabolic acidosis
- Anaemia
- Smoking - cessation as smoking increases proteinuria and CKD progression
- Glycaemic control (if diabetic) - control of blood sugar
