Kidney Flashcards by Zohaa Qaisar

What are the indications for starting dialysis? (4)

Hyperkalaemia
Uraemia
Metabolic acidosis
Pulmonary oedema

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When do you start dialysis in an anuric patient?

Only when they have indications

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What complications can uraemia cause? (2)

Encephalopathy
Pericarditis

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What is the pathophysiology of rhabdomyolysis?

Breakdown of muscle → release of CK

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What is the key investigation in rhabdomyolysis?

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What is unique about the dipstick result in rhabdomyolysis?

+ve for blood but when observed under microscope there will be no RBCs - myoglobin

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Why is rhabdomyolysis dangerous for the kidneys?

Risk of ARF as myoglobin is nephrotoxic

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What is the management of rhabdomyolysis?

0.9% saline

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What is the best measure of kidney function and what’s the normal value?

GFR = best measure of kidney (normal = 120ml/min)

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How do we estimate GFR?

Using clearance - volume of plasma cleared of a marker substance per unit time

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What is the formula for clearance?

Clearance = (urinary concentration of marker x volume) / plasma concentration of the marker

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What are the 3 criteria for using a marker to estimate GFR? (3)

Freely filtered
Not bound to plasma proteins
Not reabsorbed / secreted by tubules

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What is the gold-standard marker of GFR and why isn’t it used clinically?

Inulin is the gold-standard marker
Not used in clinical practice - requires an IV steady-state infusion

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What are the characteristics of blood urea as a marker? (4)

Endogenous marker (by-product of protein metabolism)
Freely-filtered by variable reabsorption by tubular cells
Dependent on nutrition, GI bleeding, hepatic function
Not used as a marker of GFR but of dehydration

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What are the key points about serum creatinine? (3)

Derived from muscle cells
Freely filtered, active secretion into tubules
CKD-EPI equation uses creatinine clearance to calculate eGFR - this is what we use in clinical practice

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What are the characteristics of Cystatin C? (3)

Alternative endogenous marker to creatinine - generated by nucleated cells
Freely filtered, but almost completely reabsorbed
Not really used clinically

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What is the gold standard for measuring proteinuria?

spot urine protein:creatinine ratio

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Is 24-hour urine collection commonly used for measuring proteinuria?

What is the gold standard imaging for kidney stones?

CTKUB (CT Kidneys, Ureters, Bladder)

What is the basic definition of AKI?

Reduction in GFR over 1 week - reversible

What are the three main categories of AKI? (3)

Pre-renal
Renal
Post-renal

What is the main mechanism of pre-renal AKI?

Reduced renal perfusion

What are the causes of pre-renal AKI? (7)

Shock
Renal artery stenosis
Haemorrhage
Hypotension
Calcineurin inhibitors
NSAIDs/ACIs/ARBs
Diuretics

What are the two key adaptive mechanisms that maintain renal perfusion? (2)

Myogenic stretch - afferent arteriole if stretched constricts to reduce high pressure to the bowman’s capsule
Tubuloglomerular feedback - high Cl- in the distal tubule → constriction of afferent arteriole

What are the key characteristics of pre-renal AKI? (3)

* NO structural renal damage * Responds immediately to restoration of circulating volume * Often precipitated by starting an ACEi

What is pre-renal AKI often precipitated by?

ACEi

What is the key characteristic of renal AKI?

Structural renal damage is present

What are the causes of renal AKI? (8) (MAGIC VAD)

* M - Multiple Myeloma & Myoglobin * A - Amyloidosis & ATN * G - Glomerulonephritis * I - Interstitial disease * C - Contrast * V - Vasculitis * A - Aminoglycosides, Amphotericin, Aciclovir * D - Drugs (other nephrotoxic)

What is the most common cause of ATN?

Most commonly caused by prolonged pre-renal AKI → ischaemic injury

What are the obstructive causes of post-renal AKI? (4)

- Renal stone * BPH * Transitional cell carcinoma * Extrinsic mass pressing on ureter

What happens if post-renal AKI is managed quickly vs slowly? (2)

* If managed quickly - restore GFR with no structural damage * If managed slowly - glomerular ischaemia & tubular damage

What are the causes of CKD? (6)

* DM (most common) * Hypertension * Atherosclerosis * Chronic glomerulonephritis * Prostate disease * PCKD

Most common cause of CKD?

Diabetes

What are the metabolic consequences of CKD? (4)

* Metabolic acidosis * Hyperkalaemia * Normochromic anaemia * Secondary/tertiary hyperparathyroidism

What are the major complications of CKD? (4)

* Uraemia (leading to cardiomyopathy, encephalopathy) * Renal osteodystrophy * CVD (most likely to kill them, highly calcified plaques) * Bone disease

What are the three types of bone disease in CKD? (3)

* Osteitis fibrosa cystica → bone cysts, Brown's tumours * Adynamic bone disease - resistance to PTH in bones → low bone turnover * Osteomalacia - inadequate mineralisation of bone

What are the 6 key aspects that need management in CKD? (6) Remember "AH HMVP" (Ah, Help My Vitamin P!)

* A - Anaemia * H - Hyperkalaemia * H -Hyperparathyroidism * M - Metabolic acidosis * V - Vitamin D deficiency * P - Phosphate (Hyperphosphataemia)

How is metabolic acidosis managed in CKD?

Oral sodium bicarbonate

What is the management for hyperkalaemia in CKD?

Dietary management

How is anaemia managed in CKD?

Artificial EPO (Erythropoietin)

What are the two approaches to managing hyperphosphataemia in CKD? (2)

- Dietary management * Phosphate binders

How is Vitamin D deficiency managed in CKD?

1-alpha calcidol

How is hyperparathyroidism managed in CKD?

Cinacalcet - increases sensitivity of calcium sensing receptors → decreased PTH