renal Flashcards

1
Q

what type of patients present with AKI

A

unwell patients with infection or following a surgery, above 65.

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2
Q

The NICE guidelines (2019) criteria for diagnosing an acute kidney injury are:

A

Rise in creatinine of more than 25 micromol/L in 48 hours
Rise in creatinine of more than 50% in 7 days
Urine output of less than 0.5 ml/kg/hour over at least 6 hours

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3
Q

name some of the risk factors that would predispose to developing acute kidney injury

A

Older age (e.g., above 65 years)
Sepsis
Chronic kidney disease
Heart failure
Diabetes
Liver disease
Cognitive impairment (leading to reduced fluid intake)
Medications (e.g., NSAIDs, gentamicin, diuretics and ACE inhibitors)
Radiocontrast agents (e.g., used during CT scans)

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4
Q

name the stages of renal impairment

A

Pre-renal causes are the most common. Insufficient blood supply (hypoperfusion) to kidneys reduces the filtration of blood. This may be due to:

Dehydration
Shock (e.g., sepsis or acute blood loss)
Heart failure

Renal causes are due to intrinsic disease in the kidney. This may be due to:

Acute tubular necrosis
Glomerulonephritis
Acute interstitial nephritis
Haemolytic uraemic syndrome
Rhabdomyolysis

Post-renal causes involve obstruction to the outflow of urine away 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
Tumours (e.g., retroperitoneal, bladder or prostate)
Strictures of the ureters or urethra
Benign prostatic hyperplasia (benign enlarged prostate)
Neurogenic bladder

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5
Q

what are some pre-renal kidney issues

A

insufficient blood flow-hypoperfusion, due to dehydration, heart failure, shock-sepsis, or acute blood loss.

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6
Q

what are some Renal kidney issues

A

Due to intrinsic factors:
- Acute tubular necrosis
- Glomerulonephritis
Acute interstitial nephritis
Haemolytic uraemic syndrome
Rhabdomyolysis

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7
Q

what are some post-renal kidney issues

A

obstruction to the outflow of urine away 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
Tumours (e.g., retroperitoneal, bladder or prostate)
Strictures of the ureters or urethra
Benign prostatic hyperplasia (benign enlarged prostate)
Neurogenic bladder

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8
Q

name the common cause of intrinsic renal impairments and the diagnosis of it.

A

Acute tubular necrosis- this is due to ischaemia and poor perfusion of the epithelial cells of the renal tubules
Nephrotoxins-gent, radiocontrast agents or cistplatin

  • Urinalysis- muddy brown cast, renal tubular epithelial cells may also been seen. they can regenerate quickly so this cause is reversible 1-3 weeks.
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9
Q

Acute tubular necrosis cause of renal impairment is reversible. True or false?

A

True, epithelial cells are able to regenerate in 1-3weeks.

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10
Q

What are urinalysis findings for AKI

A

-Leukocytes and nitrites - infection
- Protein and blood suggest acute nephritis, and infection
- glucose- diabetes

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11
Q

other than urinalysis what other tool is used for diagnosing stages of AKI

A

Ultrasound of the urinary tract assesses for obstruction when a post-renal cause is suspected.

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12
Q

what is the management for AKI prevention?
- consider causes of AKI

A

Avoiding nephrotoxic medications where appropriate
Ensuring adequate fluid intake (including IV fluids if oral intake is inadequate)
Additional fluids before and after radiocontrast agents

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13
Q

what is the treatment plan for AKI with an (underlying cause)- consider medications, invasive management

A

Treating an acute kidney injury involves reversing the underlying cause avoiding medications that may worsen and also medications that may accumulate with reduced renal impairment.

IV fluids for dehydration and hypovolaemia
Withhold medications that may worsen the condition (e.g., NSAIDs and ACE inhibitors)
Withhold/adjust medications that may accumulate with reduced renal function (e.g., metformin and opiates)
Relieve the obstruction in a post-renal AKI (e.g., insert a catheter in a patient with prostatic hyperplasia)
Dialysis may be required in severe cases

TOM TIP: Calling ACE inhibitors nephrotoxic is incorrect. ACE inhibitors should be stopped in an acute kidney injury, as they reduce the filtration pressure. However, ACE inhibitors have a protective effect on the kidneys long-term. They are offered to certain patients with hypertension, diabetes and chronic kidney disease to protect the kidneys from further damage.

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14
Q

Name some complications of AKI
(electrolytes)
(blood gas)

A

-fluid overload- heart failure and oedema
-metabolic acidosis
hyperkalemia
uraemia: leads to encephalopathy and pericarditis

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15
Q

Define CKD and how long does it have to maintain to be considered as CKD.

A

Chronic kidney disease (CKD) describes a chronic reduction in kidney function sustained over three months. It tends to be permanent and progressive.

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16
Q

Name some causes of CKD

A

Diabetes
Hypertension
Medications (e.g., NSAIDs or lithium)
Glomerulonephritis
Polycystic kidney disease

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17
Q

What are the presentations of CKD. (consider the synthesis of kidney, fluid status

A

Mostly Asymptomatic,
Pallor due to Anemia: erythropoetin is the hormone synthesised by the kidney for RBC formation.
- Fatigue
- foamy urine
-nausea
loss of appetite
oedema
pruritus
hypertension
peripheral neuropathy

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18
Q

what is the EGFR based on

A

The estimated glomerular filtration rate (eGFR) is based on the serum creatinine, age and gender. It estimates the glomerular filtration rate (the rate at which fluid is filtered from the blood into Bowman’s capsule).

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19
Q

Which investigation tool is used for proteinuria

A

Quantified with a urine albumin:creatinine ratio (ACR).

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20
Q

Which investigation tool is used for Haematuria

;;

A

Haematuria (blood in the urine) can be assessed with a urine dipstick or microscopy. Microscopic haematuria is when blood is identified on testing but not visible on inspection. Macroscopic haematuria refers to visible blood in the urine. Haematuria can indicate infection, malignancy (e.g., bladder cancer), glomerulonephritis or kidney stones.

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21
Q

what tool can be used to look for obstruction in the kidneys

A

Renal ultrasound helps identify obstructions (e.g., kidney stones or tumours) and polycystic kidney disease.

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22
Q

name some other investigations necessary to identify risk factors for CKD (consider common AKI causes)

A

Blood pressure (for hypertension)
HbA1c (for diabetes)
Lipid profile (for hypercholesterolaemia)

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23
Q

what are the components to classifying CKD?

A

Estimated glomerular filtration rate (eGFR) is sustained below 60 mL/min/1.73 m2
Urine albumin:creatinine ratio (ACR) is sustained above 3 mg/mmol
The G score is based on the eGFR. The A score is based on the albumin:creatinine ratio.
Accelerated progression is a sustained decline in the eGFR within one year of either 25% or 15 mL/min/1.73 m2.
G5- UNDER 15
A3- ABOVE 30MG/MMOL

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24
Q

What are the values of accelerated progression in CKD

A

Accelerated progression is a sustained decline in the eGFR within one year of either 25% or 15 mL/min/1.73 m2.

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25
Q

what are the complications of CKD

A

Anaemia
cardiovascular disease
Renal bone disease
end stage kidney diseases
dialysis related complications
peripheral neuropathy

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26
Q

what tool ‘equation’ can be used to estimate risk of kidney failure requiring dialysis and how many years does it estimate?

A

The Kidney Failure Risk Equation can be used to estimate the 5-year risk of kidney failure requiring dialysis.

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27
Q

The NICE clinical knowledge summaries (May 2023) suggest referral to a renal specialist when:
(consider hypertension issues, dialysis, accelerated progression, EGFR ACR) (5)

A

(EGFR AND ACR- 100)
eGFR less than 30 mL/min/1.73 m2
Urine ACR more than 70 mg/mmol
Accelerated progression (a decrease in eGFR of 25% or 15 mL/min/1.73 m2 within 12 months)
5-year risk of requiring dialysis over 5%
Uncontrolled hypertension despite four or more antihypertensives

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28
Q

Treating the underlying cause of CKD involves:

A

Optimising diabetic control
Optimising hypertension control
Reducing or avoiding nephrotoxic drugs (where appropriate)
Treating glomerulonephritis (where this is the cause)

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29
Q

What are the BP and ACR findings in patients under 80

A

The blood pressure target is less than 130/80 in patients under 80 with CKD and an ACR above 70 mg/mmol.

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30
Q

Medications that help slow the disease progression in CKD are:

A

ACE inhibitors (or angiotensin II receptor blockers)
SGLT-2 inhibitors (specifically dapagliflozin)

Decrease ACR RATIO

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31
Q

Reducing the risk of complications in CKD involves (consider meds used to treat common cause of AKI:

cardio input

A

Exercise, maintain a healthy weight and avoid smoking
Atorvastatin 20mg for primary prevention of cardiovascular disease (in all patients with CKD)

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32
Q

Management of complications of CKD involves: (blood gas impairment, blood status, renal bone disease)

A

Oral sodium bicarbonate to treat metabolic acidosis
Iron and erythropoietin to treat anaemia
Vitamin D, low phosphate diet and phosphate binders to treat renal bone disease

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33
Q

Management of end-stage renal disease involves:

A

Special dietary advice
Dialysis
Renal transplant

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34
Q

ACE inhibitors are offered to all patients with (consider common cause of AKI, ACR levels :

A

Diabetes plus a urine ACR above 3 mg/mmol
Hypertension plus a urine ACR above 30 mg/mmol
All patients with a urine ACR above 70 mg/mmol

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35
Q

what electrolyte imbalance is associated with CKD and ACE inhibitors

A

hyperkalaemia- monitor serum potassium

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36
Q

Patients with diabetes and CKD are offered what type of medications

A

Dapagliflozin is the SGLT-2 inhibitor licensed for CKD. It is offered to patients with:

Diabetes plus a urine ACR above 30 mg/mmol

Dapagliflozin is considered for patients with:

Diabetes plus a urine ACR or 3-30 mg/mmol
Non-diabetics with an ACR of 22.6 mg/mmol or above

37
Q

What type of anaemia does CKD cause and state the cause of this?

A

Healthy kidneys produce erythropoietin, a hormone that stimulates the production of red blood cells. CKD results in lower erythropoietin and a drop in red blood cell production. It causes a normocytic (normal sized) normochromic (normal colour) anaemia.
treated with erythropoiesis-stimulating agents: recombinant human erythropoietin.
Blood transfusions can sensitise the immune system (allosensitization), increasing the risk of future transplant rejection.

Iron deficiency is treated before using erythropoietin. Intravenous iron is usually given, particularly in dialysis patients.

38
Q

what are the treatments for Anaemia in chronic kidney disease?

A

Anaemia may be treated with erythropoiesis-stimulating agents, such as recombinant human erythropoietin. Blood transfusions can sensitise the immune system (allosensitization), increasing the risk of future transplant rejection.

Iron deficiency is treated before using erythropoietin. Intravenous iron is usually given, particularly in dialysis patients.

39
Q

How does CKD cause renal bone disease?
consider the function of kidneys in bone synthesis

A
  • high serum phosphate as a result of poor excretion
  • low vitamin D due to kidney’s inability to metabolise vitamin D into active vitamin D which is essential for calcium absorption in the intestines and reabsorption in the kidneys. It is also responsible for regulating bone turnover and promoting bone reabsorption to increase the serum calcium level. Chronic kidney disease leads to less vitamin D activity and low serum calcium.
40
Q

what type of deficiency does CKD cause?

A

Chronic kidney disease leads to less vitamin D activity and low serum calcium.

41
Q

which glands are responsible for responding to low calcium serum as a result of VitD in CKD?

A

The parathyroid glands react to the low serum calcium and high serum phosphate by excreting more parathyroid hormone, causing secondary hyperparathyroidism. Parathyroid hormone stimulates osteoclast activity, increasing calcium absorption from bone.

42
Q

what is the term used to describe the increased turnover of bones without adequate calcium supply

A

osteomalacia

43
Q

***** 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 bone is not properly mineralised.

A

OSTEOSCLEROSIS

44
Q

What is the finding on spinal x-ray for patients with renal bone disease as a result of CKD.

A

Rugger jersey spine is a characteristic finding on a spinal x-ray. This involves sclerosis of both ends of each vertebral body (denser white) and osteomalacia in the centre of the vertebral body (less white). The name refers to the stripes found on a rugby shirt.

45
Q

what are 3 disease common conditions associated with renal bone diseases

A

-Osteoporosis can exist alongside renal bone disease and may be treated with bisphosphonates.
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 bone is not properly mineralised.

46
Q

Management of renal bone disease involves a combination of:

A

Low phosphate diet
Phosphate binders
Active forms of vitamin D (alfacalcidol and calcitriol)
Ensuring adequate calcium intake

47
Q

why is there a raised ALP in CKD

A

Serum ALP level reflects bone activity, including bone turnover and bone metabolism.
(CKD) patients, serum ALP level is commonly used as a surrogate marker for hyperparathyroidism and renal bone disease. Generally, an elevated serum ALP level indicates high-turnover bone disease in CKD

48
Q

what is the conditon that involves breakdown of skeletal muscles and release chemicals into the blood (injuries, immobility). Name the chemicals released and what does the cells udnergo

A

Rhabdomylolsis- Atopsosis
Myoglobin
pottasium
phosphate
CK

49
Q

name some causes of rabdomyolisis

A

Prolonged immobility, particularly frail patients who fall and spend time on the floor before being found
Extremely rigorous exercise beyond the person’s fitness level (e.g., endurance events or CrossFit)
Crush injuries
Seizures
Statins

50
Q

what are the signs and symptoms of rhabdomyolisis

A

Muscle pain
Muscle weakness
Muscle swelling
Reduced urine output (oliguria)
Red-brown urine (myoglobinuria)
Fatigue
Nausea and vomiting
Confusion (particularly in frail patients)

51
Q

what investigation is first line used to investigate rhabdo. what are the pattern like. (what other investigations also used )

A

blood test- CK, it should be less than 150 U/L but in rhabdo it can exceed 100K it rises. it rises within 12 hours and remain elevated 1-3days then falls gradually. higher the CK indicates greater risk of kidney injury.
ECG
UEs

52
Q

what does -red-brown colour in urine indicates? its seen in the conditoin where there is a breakdown of skeletal msucles (myocytes)

A

myoglobininuria.

53
Q

what is the managment for rhabdomyolysis

A

Intravenous fluids are the mainstay of treatment to correct hypovolaemia and encourage filtration of the breakdown products. Treatment of complications, particularly hyperkalaemia, is also essential.

Additional options that are debatable and have associated risks include:

Intravenous sodium bicarbonate (to increase urinary pH and reduce the toxic effects of myoglobinuria)
Intravenous mannitol (to increase urine output and reduce oedema)

54
Q

what does HUS mean and name the cause of it. what is the classic triad.

A

thrombosis in the blood vessels triggered by shiga toxins from either E.coli 0157 or shigella.
microangiopathic haemolytic anaemia. the clots cause the red blood cells that pass through to rupture.
aki- blood flow to the kidney is affected vt thrombi and damaged RBC.
thrompocytopenia- formation of clots results in this.

55
Q

what is the presentation for HUS (10)

A

Jaundice- Haemolysis
Pallor- Aneamia
fever
Abdo pain
bruising
hypertension
lethargy
haematuria
confusion
oliguria

56
Q

what is the management for HUS

A

medical emergency and requires hospital admission:
treat hypertension, hypovalemia, severe aneamia, RF.

57
Q

what are the complications of hyperkalaemia:

A

arrythima, VF

58
Q

what are some causes of hyperkalemia

A

Rhabdomyolisis,
medications such as ACE
AKI
CKD 4/5
Adrenal insufficiency
tumor lysis syndrome

59
Q

what medications can cause hyperkalaemia

A

ACEi
aldosterone antanogist
NSAIDS
ARBS

60
Q

Hyperkalemia on blood test may not be accurate. True or false

A

haemolysis can create falsely elevated pottasium (Pseudohyperkalemia)

61
Q

what are the ECG changes found

A

Tall peaked T-waves
Prolonged PR interval
Broad QRS complex
flattened or P waves

62
Q

what is the management for hyperkalaemia for serum K below 6.5 without ECG changes

A

treat the underlying cause: treat AKI and stop medications that may contribute

63
Q

what are the values for normal mild moderate severe hyperkalemia

A

Normal: 3.5-5.3
mild 6.3-6
moderate 6-6.5
severe over 6.5

64
Q

when is it considered urgent treatment for hyperkalaemia (2)

A

ECG changes
serum K over 6.5

65
Q

explain the use of treatment for hyperkalaemia (not for lowering serum K)

A

insulin and dextrose infusion and IV calcium gluconate:
-insulin: drives pottasium from extracellular to intracellular
Dextrose : insulin secretion can lead to hypo
calcium gluconate: stabilise cardiac muscles and reduce risk of arrythmias

66
Q

what other main treatment for lowering serum potassium

A

-nebulised salbutamol- drives K into cells
-oral calcium resonium- reduce K absorption in the GI.
-sodium bicarbonate (in acidotic patient on renal device drives K into cells as it corrects the acidosis
-Hameodialysis- on persistent cases

67
Q

what is polycystic kidney disease:

A

It’s a genetic condition where healthy kidney tissue is replaced with fluid-filled cysts. The enlarged kidneys may be palpable on examination and it leads to renal failure.

68
Q

what genes are affected in autosomal dominant ADPKD

A

PKD1 gene on chromosome 16 (85% of cases)
PKD2 gene on chromosome 4 (15% of cases)

69
Q

what are the extra-renal manifestation:

A

Cerebral aneurysms
Hepatic, splenic, pancreatic, ovarian and prostatic cysts
Mitral regurgitation
Colonic diverticula

70
Q

what are some complications of ADPKD

A

hypertension
gross haematuria if cyst rupture
chronic loin/flank pain
recurrent UTI
Renal stones
end-stage renal failiure

71
Q

What is ARPKD. when is the diangosis picked up on.

A

Its caused by a mutation in the polysystic kideny and hepatic disease 1 gene on chromose 6. it is more severe and rare than autodominant.
diagnosed during antenatal scans with oligohydraminos. (reduced amniotic fluid volume due to reduced urine output.

72
Q

what is oligohydraminos

A

Oligohydramnios leads to underdevelopment of the fetal lungs (pulmonary hypoplasia) and respiratory failure shortly after birth. Patients may require haemodialysis within the first few days of life. They may have dysmorphic features, such as underdeveloped ear cartilage, low-set ears and a flat nasal bridge. End-stage renal failure usually occurs before reaching adulthood.

73
Q

what tool is used to diagnosis polycystic kidney disease.

A

Ultrasound and genetic testing.

74
Q

what tablet slows down the cyst development and progressional of renal failure in autosomal dominant PKD.

A

Tolvaptan- a vasopressin receptor antagnonsit.

75
Q

what are the management involved in ADPKD

A

√= Oligohydramnios leads to underdevelopment of the fetal lungs (pulmonary hypoplasia) and respiratory failure shortly after birth. Patients may require haemodialysis within the first few days of life. They may have dysmorphic features, such as underdeveloped ear cartilage, low-set ears and a flat nasal bridge. End-stage renal failure usually occurs before reaching adulthood.

76
Q

what is renal tubular acidosis and what are the causes of acidosis. RAAS(4)

A

type 1: distal tube cannot excrete H+ ions therefore PH high and serum pottasium high
type 2 : proximal tubule cannot reabsorb bicarb so PH high and serum pottasium low
type 4: (most common) low aldosterone or impaired aldosterone function so low urinary PH and high potassium.
type 1 and 4 involves low excretion of hydrogen in distal tubules.

bicrb and potassium same relationship

77
Q

how does type 4 RTA cause metabolic acidosis and hyperkalemia

A

Absence of alodsterone means less absorption of sodium and less secretion of potassium and hydrogen ions. therefore urine becomes acidotic still because ammonia is also made in the distal tube and act acts as a buffer there to neutralise for the acid present. However potassium supresses ammonia production and urine becomes acidotic. \
so you end uo with metabolic acidosis
hyperkalemia and low urinary PH.

Hormones such as aldosterone and angiotensin II can influence ammonia handling by the distal tubule. Aldosterone increases the activity of H⁺-ATPase in intercalated cells, enhancing H⁺ secretion and subsequent NH₄⁺ formation.

78
Q

what could be the cause of low aldosterone activity

A

adrenal insufficiency
diabtetic neuropathy
medications (ACEi spiro or epeleone.

79
Q

what is the relation between potassium and H+

A

They are interchangeable. therefore bicarb is used to treat hyperkalemia and neutralise the acididty.

80
Q

Name the drug used for aldosterone deficiency and the group

A

fludrocortisone (mineralocorticoid)

81
Q

what is glomerulonephritis

A

Glomerulonephritis describes the pathology that occurs in various diseases rather than being a disease. Treatment is targeted at the underlying cause and often involves supportive care and immunosuppression (e.g., corticosteroids).

82
Q

whats the difference between nephrotic and nephritic syndrome

A

nephrotic syndrome is when the gloemeruli do not filter properly the albumin.
Nephritic syndrome is the inflamed glomeruli do not filter properly the RBC and so haematuria is seen in urine.

83
Q

what are the features of nephritic syndrome

A

haematuria
oliguria
proteinuria
fluid retention but often less protein found than nephrotic. if the protein is higher the consider nephrotic syndrome

83
Q

what are the features of nephrotic syndrome

A

when basement membrane in the glomerulus become highly permeable and result in porteinuria.

preoteinuria- frothy urine
low albumin
perirpheral odema
hypercholestrolaemia

84
Q

what are the causes of nephrotic syndrome in adults and children

A

Adult- membranous nephropathy
- focal segmental glomerulosclerosis, diabetes, infections -HIV HSP
chidlren- idiopathic, treated sucessfully with steroids

85
Q
A
86
Q
A
86
Q
A