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FinalMB Part I - Medicine > Renal > Flashcards

Flashcards in Renal Deck (121)
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What is acute kidney injury (AKI) and how is it diagnosed ?

Its is defined as an acute drop in kidney function. It is diagnosed by measuring the serum creatinine.


NICE criteria for diagnosing AKI ?

Use any of the following:
-Rise in creatinine of 26 micromol/L or greater within 48 hrs
-Rise in creatinine of 50% or more in 7 days
-Urine output of < 0.5ml/kg/hour for more than 6 hours


Consider the possibility of an AKI in pts that are suffering with an acute illness, such as infection or having a surgical operation. Risk factors that would predispose to developing AKI include ?

-Heart failure
-Liver disease
-Older age (above 65 years)
-Cognitive impairment
-Nephrotoxic medications such as NSAIDS and ACE inhibitors
-Use of a contrast medium such as during CT scans



Whenever someone asks you the causes of renal impairment always answer "the causes are pre-renal, renal or post-renal". This will impress them and allow you to think through the cases more logically.


Pre-renal causes of AKI ?

Pre-renal pathology is the most common cause of acute kidney injury. It is due to inadequate blood supply to the kidneys reducing the filtration of blood. Inadequate blood supply may be due to:
-Hypotension (shock)
-Heart failure


Renal causes of AKI ?

This is where intrinsic disease in the kidney is leading to reduced filtration of blood. It may be due to:
-Interstitial nephritis
-Acute tubular necrosis


Post renal causes of AKI ?

Post renal AKI is caused by obstruction to outflow of urine from the kidney, causing back-pressure into the kidney and reduced kidney function. This is called an obstructive uropathy. Obstruction may be caused by:
-Kidney stones
-Masses such as cancer in the abdomen or pelvis
-Ureter or urethral strictures
-Enlarged prostate or prostate cancer


Investigations for AKI ?

Urinalysis for protein, blood, leucocytes, nitrites and glucose:
-Leucocytes and nitrites suggest infection
-Protein and blood suggest acute nephritis (But can be positive in infection)
-Glucose suggests diabetes

US of the urinary tract is used to look for obstruction. It is not necessary if an alternative cause is found for the AKI.


Management of AKI ?

Prevention of AKI is important. This is achieved by avoiding nephrotoxic medications where possible and ensuring adequate fluid input in unwell pts, including IV fluids if they are not taking enough orally.

The first step to treating AKI is to correct the underlying cause:
-Fluid rehydration with IV fluids in pre-renal AKI
-Stop nephrotoxic medications such as NSAIDS and antihypertensives that reduce the filtration pressure (i.e. ACE inhibitors)
-Relieve obstruction in post-renal AKI, for example insert a catheter for a pt in retention from a large prostate.

In severe AKI, where there is doubt about the cause or where complications develop, input from a renal specialist is required. They may need dialysis.


Name 4 complications of AKI ?

-Fluid overload, heart failure and pulmonary oedema
-Metabolic acidosis
-Uraemia (high urea) can lead to encephalopathy or pericarditis.


What is chronic kidney disease ?

CKD describes a chronic reduction in kidney function. this reduction in kidney function tends to be permanent and progressive.


Causes of CKD ( 6 bullet points) ?

-Age related decline
-Polycystic kidney disease
-Medications such as NSAIDs, PPIs and lithium


Name 5 risk factors for CKD

-Older age
-Use of medications that affect the kidneys


Presentation of CKD ?

Usually CKD is asymptomatic and diagnosed on routine testing. A number of signs and symptoms might suggest CKD:
-Pruritis (itching)
-Loss of appetite
-Muscle cramps
-Peripheral neuropathy


Investigations for CKD ?

-eGFR can be checked using a U&E blood test. Two tests are required 3 months apart to confirm a diagnosis of CKD
-Urine albumin:creatinine ratio (ACR) can be used to check for proteinuria. A result of ≥ 3mg/mmol is significant.
-A urine dipstick can be used to check for haematuria. A significant result is 1+ of blood. Haematuria should prompt investigation for malignancy (i.e. bladder cancer)
-Renal US can be sued to investigate pts with accelerated CKD, haematuria, FH of polycystic kidney disease or evidence of obstruction


Staging CKD : G score ?

The G score is based on the eGFR:

G1 = eGFR>90
G2 = eGFR 60-89
G3a = eGFR 45-59
G3b = eGFR 30-44
G4 = eGFR 15-29
G5 = eGFR < 15 (known as "end-stage renal failure"


Staging CKD: A score ?

The A score is based on the albumin:creatinine ratio:

A1= < 3mg/mmol
A2 = 3-30mg/mmol
A3 = > 30mg/mmol


When would a pt not have CKD/ have CKD ?

The pt does not have CKD if they have a score of A1 combined with G1 or G2. They need at least an eGFR of less than 60 (G3a and above) or proteinuria for a diagnosis of CKD.


Name 5 complications of CKD ?

Renal bone disease
Cardiovascular disease
Peripheral neuropathy
Dialysis related problems


When do NICE suggest referral to a specialist in CKD ?

Any of the following:
-eGFR < 30
-ACR ≥ 70mg/ mmol
-Accelerated progression defined as a decrease in eGFR of 15 or 25% or 15ml/min in 1 year
-Uncontrolled HTN despite 4 or more antihypertensives


Aims of management of CKD ?

-Slow the progression of the disease
-Reduce the risk of cardiovascular disease
-Reduce the risk of complications
-Treating complications


Management of CKD (use headings) ?

Slowing the progression of the disease:
-Optimise diabetic control
-Optimise hypertensive control
-Treat glomerulonephritis

Reducing the risk of complications:
-Exercise, maintain a healthy weight and stop smoking
-Special dietary advice about phosphate, sodium, potassium and water intake.
-Offer atorvastatin 20mg for primary prevention of cardiovascular disease

Treating complications:
-Oral sodium bicarbonate to treat metabolic acidosis
-Iron supplementation and erythropoietin to treat anaemia
-Vit D to treat renal bone disease
-Dialysis in end stage renal failure
-Renal transplant in end stage renal failure


Treating HTN in CKD ?

ACEi are the first line in pts with CKD. These are offered to all pts with:
-Diabetes plus ACR > 3mg/mmol
-HTN plus ACR > 30mg/mmol
-All pts with ACR > 70mg/mmol

Aim to keep BP < 140/90 (or 130/80 if the ACR > 70mg/mmol)

Serum potassium needs to be monitored as CKD and ACEi both cause hyperkalaemia.


How can CKD cause anaemia ?

Healthy kidney cells produce erythropoiein. Erythropoietin is the hormone that stimulates production of red blood cells. Damaged kidney cells in CKD cause a drop in erythropoietin Therefore, there is a drop in RBCs and a subsequent anaemia.


How can anaemia of CKD be treated ?

With erythropoiesis stimulating agents, such as exogenous erythropoietin. Blood transfusions should be limited as they can sensitise the immune system ("allosensitisation") so that transplanted organs are more likely to be rejected.


What should be treated before offering EPO in anaemia of CKD, with what and why does this happen ?

Iron deficiency should be treated before offering EPO. IV iron is usually given, particularly in dialysis pts. Oral iron is an alternative. This happens as CKD causes a rise in hepcidin which reduces iron absorption from the GI tract.


What is renal bone disease also known as ?

Chronic kidney disease-mineral and bone disorder (CKD-MBD)


Features of renal bone disease ?



Xray changes of renal bone disease ?

Spinal xray shows sclerosis of both ends of the vertebra (denser white) and osteomalacia in the centre of the vertebra (less white). This is classically known as "rugger jersey" spine after the stripes found on a rugby shirt.


Pathophysiology of renal bone disease ?

HIGH SERUM PHOSPHATE due to reduced phosphate excretion. LOW ACTIVE VIT D occurs because the kidney is essential in metabolising vit D to its active form. ACTIVE VIT D is essential in calcium absorption from the intestines and kidneys, therefore there is a low serum calcium. Vit D also regulates bone turnover.

SECONDARY HYPERPARATHYROIDISM occurs because the PT glands react to the low serum calcium and high serum phosphate by excreting more PTH. This leads to increased osteoclast activity. Osteoclast activity leads to the absorption of calcium from bone.

OSTEOMALACIA occurs due to increased turnover of bones without adequate calcium supply

OSTEOSCLEROSIS occurs when the osteoblasts respond by increasing their activity to match the osteoclasts, creating new tissue in the bone. Due to the low calcium level this new tissue is not properly mineralised.

OSTEOPOROSIS can exist alongside the renal bone disease due to other risk factors such as age and use of steroids.