CKD Flashcards

1
Q

Definition?

A

Chronic kidney disease (CKD), also known as chronic renal failure, is defined as abnormalities of kidney structure or function, present for ≥3 months, with implications for health.

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2
Q

RF?

A
  • DM
  • HT
  • Age>50
  • Childhood kidney disease
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3
Q

ddx?

A

Ddx Findings
Diabetic kidney disease Poorly controlled diabetes, existing complications, HbA1c,microalbumin, GFR, KUS
Hypertensive nephrosclerosis Poorly controlled hypertension, microalbumin, GFR, KUS,
Ischaemic nephropathy Suddenly uncontrolled, history of atherosclerotic disease, obstructions on KUS, narrowing of renal artery
Obstructive uropathy Prostatic enlargement, urinary signs, hydro nephrosis and post-void residual vol in cases of obstruction
Nephrotic syndrome Sudden onset of hypertension, periorbital/peripheral oedema, hypoalbuminemia, hyperlipidaemia, increase in serum creatinine, serology for secondary causes
Glomerulonephritis Sudden onset of hypertension, autoimmune disorder signs, increased creatinine, haematuria and proteinuria, serology

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4
Q

epidemiology?

A

Age: >50
Sex: -
Ethnicity: Black, Hispanic
P:estimated that 9% to 13% of the adult population worldwide has CKD

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5
Q

Aetiology?

A
• Diabetic nephropathy
• Hypertensive nephropathy
• Glomerulonephritis
• Polycystic kidney disease
• Urological disease
• Amyloidosis
• Toxins
Chronic inflammation
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6
Q

CP?

A
  • Patients areoften asymptomatic until later stages.
  • Hypertension
  • Peripheraledema
  • Pulmonary edema(usuallyinterstitialpulmonary edema)
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7
Q

CP uraemia?

A

• Fatigue, weakness, loss of appetite,headaches
○ Uremic fetor
• Pigmented spots
• Pruritus
• Anemia
• Uremic pericarditis
○ Friction rub onauscultation
○ Diagnostics:Uremic pericarditisdoes not show typicalECGchanges such as diffuseST-segmentelevation.
• Pleuritis
• Asterixis
• Encephalopathy:seizures,somnolence,coma
• Peripheral neuropathy:paresthesias
• Gastrointestinal symptoms:nausea, vomiting
• ↑ Riskof infection:leukocytedysfunction
• ↑ Bleeding tendencysecondary toplatelet dysfunction

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8
Q

renal signs of ADPKD?

A
  • Gross hematuria
    • Flank or abdominalpain
    • Recurrent urinary tract infections
    • Nephrolithiasis
    • Kidneysmight be palpable and enlarged onabdominal exam(they are usually normal atbirth)
    • Signs ofchronic kidney disease(e.g.,hypertension, fluid overload,uremia)
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9
Q

Extra-renal signs of ADPKD?

A

• Multiple benignhepatic cysts(prevalenceincreases with age)
• Cysts may also occur in thepancreas,spleen,ovary, andtesticles.
• Cerebralberry aneurysm(∼8%)[13]
○ The risk is higher in patients with afamily historypositive ofADPKD.
○ May rupture and causesubarachnoid hemorrhage(the risk for growth and rupture is the same in patients withADPKDas in the general population)
• Cardiovascular
○ Signs ofarterial hypertension(e.g., morningheadaches)through increasedreninproduction
○ Heart valvedefects (particularlymitral valve prolapse)
○ Left ventricular hypertrophy
○ Potential association withcoronary arteryaneurysmandaortic aneurysm
• Colondiverticula(diverticulosis), abdominal oringuinal hernias

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10
Q

P?

A
  • Kidneys regulate waste, electrolytes and water content and make hormones
  • Renal artery forms glomeruli that filter out blood of its contents
  • Filtrate formed moves out into renal tubule-GFR (100-120ml/min/1.73m2)
  • Hypertension-walls of renal arteriole thicken against pressure-narrow lumen-less blood and oxygen to kidney-ischaemia to glomerulus-macrophages and neutrophils are attracted to the site of ischaemia and release growth factors (TGF-B1
  • Mesangial cells in glomerulus regress back to mesangioblasts and secrete ECM-glomerulosclerosis
  • This impairs the ability to filter the blood
  • Diabetes-excess glucose in the blood sticks to proteins (non-enzymatic glycation) making the efferent arteriole harder-hyaline arteriosclerosis-harder for blood to leave glomerulus-increased pressure and difficulty for things to leave causes hyperfiltration of the blood
  • Mesangial cells secrete mroe ECM-expansion of glomerulus-glomerulosclerosis affects ability to filter blood and leads to CKD
  • Less filtration-more urea in blood-azotemia-causes nausea and loss of appetite, asterixis due to encepahlopathy, pericarditis, less clot formation (inhibits platelets sticking to each other), ureamic frost (build up in skin)
  • Hyperkalaemia-arrhythmias
  • Hypocalcaemia-less vitD is made-More PTH-bones lose calcium-brittle-renal osteodystrophy
  • Falling GFR-increased renin-higher BP-more VC
  • Less erythropoietin-less RBC production-anaemia
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11
Q

First line investigations?

A

exam
blood
urine
imaging-us kub

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12
Q

Second line investigations?

A

Histology

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13
Q

Classification?

A
G1	≥90	Normal or high
G2	60-89	Mildly decreased*
G3a	45-59	Mildly to moderately decreased
G3b	30-44	Moderately to severely decreased
G4	15-29	Severely decreased
G5	<15	Kidney failure

A1 <30 Normal to mildly increased
A2 30-300 Moderately increased*
A3 >300 Severely increased**

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14
Q

First line management all?

A

• Diet
• Salt restrictionin patients withedemaorhypertension
• See treatment ofhyperkalemia.
• See treatment ofacid-base disorders.
• Nephrotoxic substancesavoidance
• NSAIDs
• Nicotine
• Sulfonamideantibiotics,aminoglycosides,vancomycin
• Acyclovir
• Cisplatin
• Others (e.g., lead,amphetamines,amphotericin B, radiographic contrast material)
• Strict blood pressure control
• Well-controlledblood pressure is essential to prevent disease progression.
• See treatment ofhypertension.
• Vaccinations
• All patients with CKD
○ Pneumococcal vaccineevery5 years
○ Influenza vaccineannually
• Susceptible patients:hepatitis Bvaccine(seehigh-risk groups for HBV infection)

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15
Q

G1-G2 management?

A
First line:
ACEi or ARB
	If
	• dmanda:cr>3mg/mmol.
	• Hypertension anda:cr>30mg/mmol.
	• Anyckdwitha:cr>70mg/mmol.
	• Check K+and renal function prior to, and 1–2 weeks after, starting treatment or changing dose. Stop if K+>6mmol/L, ↓egfr>25%, or ↓creatinine >30%: exclude other possible causes and consider a lower dose.
Statin
Antihypertensive therapy-
	Target systolicbpis <140mmHg (range 120–139mmHg) and diastolic <90mmHg. Ifdmora:cr>70 then systolic target is <130mmHg (range 120–129) and diastolic <80mmHg.
Glycaemic control-53 mmol/mol
Second line:
Non-dihydropyridine calcium-channel blocker
Statin
Antihypertensive therapy
Glycaemic control
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16
Q

G3-G4 management?

A

ACEi or ARB
Statin
Antihypertensive therapy
Glycaemic control

Non-dihydropyridine calcium-channel blocker
Statin
Additional antihypertensive therapy
Glycaemic control
Erythropoietin-stimulating agent and iron if anaemic
Diet, phosphate binders, ergocalciferol, active vitD analogue if Secondary hyperparathyroidism
Oral sodium bicarbonate if metabolic acidosis

17
Q

G5 management?

A

Dialysis
Kidney Transplant
Diet, phosphate binders, ergocalciferol, active vitD analogue if Secondary hyperparathyroidism

18
Q

When do we refer?

A
late stages
proteinuria
declining eGFR
low eGFR for a yr
high BP
genetic cause
19
Q

Prognosis?

A
  • CKD is mostly progressive and leads to end-stage renal disease (ESRD) and the need for renal replacement therapy (i.e., dialysis, transplant). Though it cannot be cured, it can be controlled and managed to a large extent.
  • Glycaemic control and hypertensive control are good prognostic factors
20
Q

Complications?

A
  • Anaemia
  • Renal osteodystrophy
  • CVD
  • Protein malnutrition
  • Metabolic acidosis
  • Hyperkalaemia
  • Pulmonary oedema