AKI CKD and other renal disease

Question 1

What is the definition of AKI? What characterises AKI?

Answer 1

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.

Question 2

What are the symptoms of AKI?

Answer 2

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
  *

Question 3

How many stages are there to AKI and how can they be classified?

Answer 3

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

Question 4

List causes of pre-renal AKI.

Answer 4

Pre-renal causes are typically underperfusion. Hypovolemia (dehydration), Sepsis, Renal artery stenosis/sclerosis, cardiac failure

Question 5

List causes of intra-renal AKI.

Answer 5

Ischaemia, nephrotoxins, pyelonephritis, trauma, early stage inflammatory conditions for CKD

Question 6

List causes for post-renal AKI.

Answer 6

Renal calculi, renal cancer, prostatic hypertrophy

Question 7

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

Answer 7

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.

Question 8

What is the turning point for fluid replacement therapy killing or curing patients?

Answer 8

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.

Question 9

Severe renal failure can lead to a metabolic acidosis. What are the signs and symptoms of a metabolic acidosis?

Answer 9

Hyperkalaemia, malaise, nausea, hyponatraemia, fluid overload.

Question 10

Which is better marker of renal function in end stage renal disease: eGFR or creatinine? Why?

Answer 10

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

Question 11

Why do CKD patients develop anaemia?

Answer 11

Because of reduced erythropoietin production

Question 12

Why do CKD patients develop secondary hyperparathyroidism?

Answer 12

Because there is reduced 1 alpha hydroxylation of vitamin D which leads to hypocalcaemia.

Question 13

What are the albuminuria stages used for classifying CKD?

Answer 13

ACR

<30mg/g

30-300mg/g

>300mg/g

Question 14

What are the stages of eGFR used for classifying CKD?

Answer 14

G1- >90 G2- 60-89 G3A- 45-59 G3B- 30-44 G4- 15-29 G5- <15

Question 15

Why do CKD patients have an increased risk of CHD?

Answer 15

Elevated cholesterol and triglyceride

Question 16

How will water balance be altered in glomerular damage? What may be an example of this?

Answer 16

There will be little glomerular filtrate and so oliguria and fluid overload will develop. Glomerulonephritis

Question 17

How will water balance be altered in a healthy nephron in a disease kidney? What may be an example of this?

Answer 17

Osmotic diuresis, polyuria. PCKD

Question 18

How will water balance be altered in tubular damage? What may be an example of this?

Answer 18

Ineffective water reabsorption leading to polyuria. Interstitial nephritis

Question 19

Name 8 features of CKD management

Answer 19

1. Alfacalcidol- Corrects hypocalcaemia
2. Erythropoietin
3. Phosphate binders to reduce risk of metastatic calcification
4. Low potassium diet
5. Lots of fluids
6. Smoking cessation
7. Blood pressure control
8. Control diabetes (if present)
9. Commence statins

Question 20

What is Fanconi syndrome?

Answer 20

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).

Question 21

What is hypophosphataemic rickets?

Answer 21

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.

Question 22

What are renal tubular acidoses?

Answer 22

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.

Question 23

What are the distinguishing features of type 1 renal tubular acidosis? How is it treated?

Answer 23

inability of the intercalated cells to excrete hydrogen ions. Hypokalaemia. Nephrolithiasis is typically present. Alkali therapy with sodium bicarbonate

Question 24

What are the distinguishing features of type 2 renal tubular acidosis? How is it treated?

Answer 24

Inability of the proximal tubule to reabsorb HCO3-. Hypokalaemia. Nephrolithiasis is absent. Alkali therapy with with potassium citrate

Question 25

What are the distinguishing features of type 4 renal tubular acidosis? How is it treated?

Answer 25

Aldosterone deficiency/resistance hyperkalaemia Furosemide, low K+ diet, fludrocortisone

Question 26

What is the triad of nephrotic syndrome?

Answer 26

Proteinuria, hyperlipidaemia, hypoalbuminemia

Question 27

What type of immune reaction is post-streptococcal glomerulo nephritis? What is the appearance under microscopy? Which complement protein is downregulated?

Answer 27

Type 3 Lumpy bumpy gloms C3

Question 28

What is the triad of nephritic syndrome?

Answer 28

HTN, haematuria, oliguria

Question 29

Draw out the oxford handbook causes of AKI

Answer 29

Question 30

Name 7 groups of patients at risk of developing AKI.

Answer 30

1. Increaseing age
2. Patients with pre-exisiting CKD
3. Patients having undergone surgery
4. Patients with DM
5. Patients with volume depletion
6. Patients on nephrotoxic drugs
7. LV dysfunction
8. Hyperbilirubinaemia and frank jaundice.

Question 31

What is renal autoregulation in the context of decreased renal blood flow? AT what level does it stop being effective and results in a significant drop in GFR?

Answer 31

GFR is initially maintained because intraglomerular pressure is preserved despite the fall in systemic BP through renal autoregulation. This is dependent on the balance between dilatation of the pre-glomerular afferent arteriole (→ prostaglandins and NO) and constriction of the efferent post-glomerular arteriole (→ mainly angiotensin II).

If perfusion continues to fall, pre-renal AKI will result. As RBF drops, so glomerular filtration and urine output fall as well. Below a mean arterial pressure (MAP) of ∼80mmHg, GFR ↓ rapidly. However, lesser degrees of hypotension may provoke pre-renal AKI in susceptible individuals:

Question 32

What is the most common cause of intrinsic AKI? What are the 2 subtypes of this?

Answer 32

ATN is, by far, the most commonly encountered cause of intrinsic AKI. It is widely seen in hospitalized patients and is predictable in high-risk clinical scenarios (so it is often preventable).

1. Nephrotoxic
2. Ischaemic

Question 33

What is the cause of ATN?

Answer 33

• Blood flow is not uniform within the kidney—pO2 falls progressively from cortex (6.65–13.3kPa) to medulla (1.3–2.9kPa) despite higher metabolic activity in the latter. ▶ The proximal tubular S3 segment and the medullary thick ascending loop of Henle are found in the medulla.
• Any cause of ↓ RBF or endothelial injury may ↓ delivered O2, rendering vulnerable segments of the nephron relatively hypoxic

Question 34

Draw out the flowchart for urine dip interpretation from oxford handbook.

1.

Answer 34

Question 35

What are the 2 imaging modalities most commonly utilised in AKI? What information can be gathered from them?

Answer 35

CXR

Perform a CXR (urgently if tachypnoea, ↓ O2 sats, haemoptysis, suspected infection, or significant associated primary lung disease).

The key findings are pulmonary oedema, respiratory infection, and pulmonary haemorrhage (all → air space shadowing that may look identical).

However, additional useful information may be gathered:

• Cardiac contour—? LVH consistent with long-standing ↑ BP, ? pericardial effusion.
• Hilar lymphadenopathy, lytic lesions.

Renal ultrasound

Perform an USS of the renal tract as soon as possible (within hours if suspected pyonephrosis).

Imaging rarely makes a specific diagnosis but has two principal aims:

• To exclude obstruction.
• To confirm the presence of two kidneys and measure renal length. Renal length is used as a surrogate for the time course of renal impairment. Long-standing CKD → parenchymal scarring, loss of renal volume and length.