AKI CKD and other renal disease Flashcards
What is the definition of AKI? What characterises AKI?
Acute kidney injury (AKI) (formerly acute renal failure) is the syndrome arising from a rapid fall in GFR (over hours to days). It is characterized by retention of both nitrogenous (including Ur and Cr) and non-nitrogenous waste products of metabolism, as well as disordered electrolyte, acid–base, and fluid homeostasis.
What are the symptoms of AKI?
The presentation is dependent on the cause and severity of AKI. Some patients are asymptomatic, but oliguria is the commonest symptom.
- There can also be N+V, dehydration, confusion.
- Hypertension
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How many stages are there to AKI and how can they be classified?
Stage 1- Creatinine increase between 1.5-1.9 baseline and <0.5ml/kg/h urine output for 6-12 hours Stage 2- Creatinine increase between 2-2.9 baseline and <0.5ml/kg/h urine output for >12h Stage 3- Creatinine increase of greater than 3 times from baseline or >353.6umol/L and 0.3ml/kg/h for 24 hours or anuria for greater than 12 hours
List causes of pre-renal AKI.
Pre-renal causes are typically underperfusion. Hypovolemia (dehydration), Sepsis, Renal artery stenosis/sclerosis, cardiac failure
List causes of intra-renal AKI.
Ischaemia, nephrotoxins, pyelonephritis, trauma, early stage inflammatory conditions for CKD
List causes for post-renal AKI.
Renal calculi, renal cancer, prostatic hypertrophy
How do the following measurements vary in pre-renal vs intra-renal damage? Urine volume, Urine:plasma osmolality, urine Na+ conc., serum Na+, urea:creatinine
Urine volume is low in pre-renal damage but initially high in intra-renal. Urine:plasma osmolality is >2:1 in pre-renal because the kidneys are trying to preserve water. Urine:plasma osmolality in intra-renal damage is 1:1 because urine conc. goes down as the kidneys are no longer functioing. In pre-renal damage the urine sodium concentration goes down and the serum sodium goes up because it is being preserved. In intra-renal damage the urine sodium is up and the serum sodium is down because it is being lost. In pre-renal damage the urea:creatinine ratio goes up due to hypoperfusion and in intra-renal damage the ratio can be normal or actually reduced.
What is the turning point for fluid replacement therapy killing or curing patients?
If a patient has a simple low perfusion problem but has not actually entered a state of AKI then fluid cures. If the patient is in AKI then fluid can kill.
Severe renal failure can lead to a metabolic acidosis. What are the signs and symptoms of a metabolic acidosis?
Hyperkalaemia, malaise, nausea, hyponatraemia, fluid overload.
Which is better marker of renal function in end stage renal disease: eGFR or creatinine? Why?
As eGFR gets very low creatinine can go up and not decrease eGFR by much. Therefore creatinine is a more sensitive marker for decreasing kidney function
Why do CKD patients develop anaemia?
Because of reduced erythropoietin production
Why do CKD patients develop secondary hyperparathyroidism?
Because there is reduced 1 alpha hydroxylation of vitamin D which leads to hypocalcaemia.
What are the albuminuria stages used for classifying CKD?
ACR
<30mg/g
30-300mg/g
>300mg/g
What are the stages of eGFR used for classifying CKD?
G1- >90 G2- 60-89 G3A- 45-59 G3B- 30-44 G4- 15-29 G5- <15
Why do CKD patients have an increased risk of CHD?
Elevated cholesterol and triglyceride
How will water balance be altered in glomerular damage? What may be an example of this?
There will be little glomerular filtrate and so oliguria and fluid overload will develop. Glomerulonephritis
How will water balance be altered in a healthy nephron in a disease kidney? What may be an example of this?
Osmotic diuresis, polyuria. PCKD
How will water balance be altered in tubular damage? What may be an example of this?
Ineffective water reabsorption leading to polyuria. Interstitial nephritis
Name 8 features of CKD management
- Alfacalcidol- Corrects hypocalcaemia
- Erythropoietin
- Phosphate binders to reduce risk of metastatic calcification
- Low potassium diet
- Lots of fluids
- Smoking cessation
- Blood pressure control
- Control diabetes (if present)
- Commence statins
What is Fanconi syndrome?
A rare renal tubular disorder characterized by a generalized defect in reabsorption in the proximal renal tubules. Causes increased excretion of glucose, phosphate, amino acids, bicarbonate, uric acid, sodium, potassium, and water. Can be hereditary (e.g., as part of inherited disorders like Wilson disease) or acquired (e.g., from drug toxicity, multiple myeloma, amyloidosis).
What is hypophosphataemic rickets?
Hypophosphataemic rickets that is caused by a hereditary overactivity of fibroblast growth factor 23 (FGF23). The most common cause (80% of cases) of hereditary hypophosphatemic rickets is an X-linked dominant mutation in the PHEX gene, which is responsible for down-regulating FGF23 activity (X-linked hypophosphatemic rickets). Less commonly, hereditary hypophosphatemic rickets is caused by an autosomal dominant mutation that makes FGF23 resistant to proteolysis, or by an autosomal recessive mutation that increases FGF23 production.
What are renal tubular acidoses?
A normal anion gap (hyperchloremic) metabolic acidosis in the presence of normal or almost normal renal function. The various types of RTA include proximal tubular bicarbonate wasting (type II), distal tubular acid secretion (type I), very rarely carbonic anhydrase deficiency (type III), and aldosterone deficiency/resistance (type IV). Renal tubular acidosis arises as a result of defects in the tubular transport of HCO3- and/or H+. Most forms of RTA are asymptomatic although, rarely, life-threatening electrolyte imbalances can occur.
What are the distinguishing features of type 1 renal tubular acidosis? How is it treated?
inability of the intercalated cells to excrete hydrogen ions. Hypokalaemia. Nephrolithiasis is typically present. Alkali therapy with sodium bicarbonate
What are the distinguishing features of type 2 renal tubular acidosis? How is it treated?
Inability of the proximal tubule to reabsorb HCO3-. Hypokalaemia. Nephrolithiasis is absent. Alkali therapy with with potassium citrate
