J de Zoysa Flashcards
What are the roles of the kidney?
Elimination of waste products
Control of fluid balance
Regulation of acid-base balance
Production of hormones - epo, vitamin D, aldostrone
Ho do you stage acute kidney injury?
Into 3 stages by serum creatinine or urine output. Can be either.
Stage 1: 1.5-1.9x baseline or an increase of >26 umol/L serum creatinine and urine output of <0.5 ml/kg/hr for 6-12 hours.
Stage 2: 2.2.0-2.9 x baseline serum creatinine or <0.5 ml/kg/or >12 hours
Stage 3: 3 x baseline, increase in Cr> 354 umol/L or Renal replacement therapy or <0.3 ml/kg/hr for >24 hours or anuria for >12 hours
What are the types of AKI?
Pre-renal
Renal
Post renal
What i the general approach to someone with AKI?
Identify those at high risk and optimise their care
Stop all nephrotoxic agents
assess and optimise volume status
Monitor creatinine and urine output.
Who is at risk of AKI?
Chronic kidney disease Age >75 Heart failure liver disease Cardiovasculardisease Diabees mellitus Polypharmacy
What meds need to be revised in AKI?
at are nephrotoxic, e.g. NSAIDs, gentamicin, anti-hypertve agents.
Meds that are renally excreted, e.g. hypoglycaemic agents
Ho do you assess the volume status of a patient?
Eyes sunken Dry mucus membranes Reduced tissue turgor JVP Oedema Heart sounds Listen t the lungs
What investigations would you do for someone with kidney?
Invasive and/ or non-invasive
Streptococcal serology
Viral serology
Bloods
Autoimmune tests
Imaging (ultrasound or CT) to look at structure of kidney and if there is any obstructions.
Renal biopsy - look at nephrons
What is chronic kidney disease AND how is it graded?
Exam
Abnormalities of kidney function or structure present for >3 months, with implications for health.
it is classified based on cause, GFR category and albuminuria category.
CKD 1: GFR >90 ml/min CKD 2: GFR 60- 90 ml/min CKD 3: GFR 30-60 ml/min CKD 4: GFR 15-30 ml/min CKD 5: GFR <15 ml/min
Albuminuria also applied:
A1: <3 mg/mmol
A2: 3-30 mg/mmol
A3: >30 mg/mmol
How do you measure GFR?
1) Clearance of artificially injected substances (inulin) - inject into the blood:
GFR = Vol of urine per time x con inulin in urine/ conc of inulin in the blood.
2) Creatinine clearance - 24 hour creatinine clearance
produced by creatin metaboliscles.
Creatinine clearance (24 hours) = urine creatinine X urine volume / plasma creatinine X time period.
Creatinine clearance depends on muscle mass Ixample, a small child and a body builder may have the same GFR by hugely different creatinine levels.
As kidney functions declines, the amount of kidney excreted in tubules increases and their is decreased muscle mass. This results in an ovresimation of GFR in patients nearing end-stage renal disease. Use a formula to take this into account. These account for gender and race.
What are the risk factors of CKI?
Age Sex (Men) Ethnicity (Maori and Pacific islander) Low income Obesity Smoking
What are the main causes of CKD?
Diabetic nephropathy
Glomerulonephritis (IgA nephropathy common)
Hypertension
Polycystic kidney disease
Why does CKD progress?
Either because of the primary disease or because of the secondary factors that develop. For example, if the cuase of CKD is diabetic nephropathy then you treat the diabetes but also the hypertension (systemic and intraglomerular hypertension), glomerular hypertrophy, calcium and phohatese, dislipidaemia, proteinuria, tubulo-interstitial fibrosis, toxicity of molecules that arent being removed (iron/amonia)
Must focus on both the primary and secondary factors.
95% of patients with CKD will develop hypertension
What do you do to help with hypertension?
Weight loss Exercise Salt restriction Moderation of alcohol Stop smoking Target of 140/80 mmHg or better
Drugs:
1) Induce naturesis (diuretics)
2) Renin: angiotensin (ACEi, Ang II receptor blockers, aldosterone antagonists)
3) SNS blockage - alpha blockers, beta blockers, calcium channel blockers
What is the issue with proteinuria in CKD?
It is a prognostic factor. Try to reduce it. Protein restriction.
It causes fibrosis in the nephrons and tubular injury.
Treat with: Weight loss ACEi/AIIRB Aldosterone antagonists Statins Moderate protein restriction BP <125/70 mmHg Quit smoking
What happens to phosphate and calcium in CKD?
It is increased (deposited) in the kidney. This is also associated with deterioration of disease.
limit phosphate in the diet. Give phosphate binders - calcium carbonate
What else do you need to do for patients with CKD?
Calcium and phosphate maintanence. Maintain the patients water balance. Maintain endocrine function: EPO, vitamin D, angiotensin maintain electrolites. Maintain electrolyte balance Maintain acid balance
Patients typically develop metabolic acidosis due to lack of excretion
addition of oral sodium bicarbonate may be required.
Treat the uraemia: seen in CKD 4 and 5.
Uraemia causes loss of appetite, anorexia, nausea, skin itch, cold.
Neurology symptoms: fatigue and lethargy, sleep disturbances, headache, seizures, encephalopathy, peripheral neuropathy, paralysis.
Haematological issues: anaemia (because of reduced EPO), bleeding, platelet dysfunction, infection
Cardiac symptoms: pericarditis, hypertension, heart failure, IHD, cardiomyopathy, CVA, PVD
Depression, anxiey
Due to multiple toxins not excreted.
No single treatment.
Correct the abnormalities - Hb, Calcium/phosphate, other electrolytes, acid/base balance, volume, renal replacement therapy
What is renal replacement therapy?
Dialysis - perotoneal, haemodialysis
Renal transplant - cadaveric or living
What is the main difference in electrolytres between ECF and ICF?
More K+ in the cell and less Na - maintained by sodium potassium ATPases
What is molarity?
The number of Moles per litre of fluid:
1 mole = 6.022x10^23
What is the osmotic concentration?
The solute concentration - number of osmols per litre of solution.
Tightly regulated by the balance of salt and water.
Hyperosmolarity is defined as too much cation and too little water
Hyposmolarity is defined as too little cation and to much water.
What is tonicity?
It refers to what happens to cells in a solution.
Where is ADH made and secreted, when is it produced and what does it do?
Made in the hypothalamus and secreted from the pituitary.
Acts on the distal convoluted tubules and collecting ducts.
There is increased production if BP falls (ANG II) or osmolarity increases (osmoreceptors).
It increases BP and reduces osmolarity
What are the features of aldosterone?
Produced in the adrenal glans. Is an mineralocorticoid hormone.
Acts on the distal convoluted tubule and collecting duc.
Increases sodium absorption and potassium excretion.
Stimulated by potassium and angiotensin 2
Where do potasium sparing diuretcs act?
On the collecting duct.
What sort of diuiretic is furosemide?
A loop diuretic
Where do thiazide diuretcs act?
On the distal tubule.
What causes hypernatraemia?
Impaired thirst/level of consciousness.
No access.
Burns/diarrhoea/blood loss
Solute diuresis (hyperglycaemia or drugs)
Can be caused by diabetes insipidus where there is a reduction in the production of ADH. -> increased water loss. This elevates the plasma osmolality. The cause can be either central (brain injury) or nephrognic (kidney or acquaporin channel problem)
If you are hyperglycaemic what will your urine osmolality?
Hypo because the glucose in the urine pulls water with it.
What is hyponatraemia?
Decreased Na. Caused by too much excretion or too much water.
What is pseudohyponatraemia?
Low Na in the blood but osmolarity is normal.
True neutopenuia causs the blood osmolality to be low.
Is caused by the movement of water from cells into the blood stream. Can occur with hypoglycaemia (increased osmolarity) or with infusion of mannitol.
Also check urine osmolality if suspect Na imbalance.
<100 mosm/kg = very very dilute
Too much water
What happens to Na levels in volume change?
Not sure about this one.
Check the volume stats.
Dehydrated - urine sodium <20 mmol/l
Sodium loss but relatively less than water loss.
- diarrhoea, vomiting
- bowel obstruction
- skin losses - burns, sweating
- urinary losses, diuretics, addisons disease, ketonuria
Can also be caused by hypervoluemia: Na retention but more water retention -cirrhosis Nephrotic syndrome heart failure Renal failure
May be euvolaemic:
- SIADH
- diuretics
- fluid replacement
What are the features of the syndrome of inapropriate ADH?
Inapropriate production in absence of normal stimuli.
Body accumulates too much water. t is stored in cells so the patient doesn’t appear to be overloaded.
urine ismil: not low - usually greater than 150 mosmol/kg
Urine sodium - not low
Plasma osmolality: low
Caused by trauma, such as surgery, chronic lung disease, medications
What are the symptoms of hypernatraemia?
Depends of speed of development
Slow -> brain adapts, confusion, not quite self
Rapid: cerebal oedema, confusion,seizures, come
What are some of the roles of magnesium?
Bone formation
It is a co-factor in many enzymatic reactions, including ATP metabolism, muscle contraction and relaxation, release of neurotransmitters
regulation of vascular tone
Cardiac rhythm
Platelet activated thrombosis
Hydration status
How is Magnesium homeostasis regulated?
Mainly through diet intake. A lot is excreted in the faeces and the rest gets into the blood. Kidneys regulate the amount of magnesium in the system. A lot will go into bone and muscle storage.
Serum Mg is controlled by its excretion in the urine. 60-70% is reabsorbed in the thick ascending limb of the loop of henle
How is magnesium absorbed in the nephron?
10-20% in the proximal convoluted tubule.
- Magnesium is absorbed through a paracellular (between cells) pathway. It moves with water and Na.
60-70% in the thick ascending limb. Paracellular movement again. Th transport proteins claudin 16 and 19 are important in this movement. Mutations in this pathway lead to stone formation, low serum Mg and Ca and get kidney failure.
10% in the distal convoluted tubule. Active process of Mg excretion.
How do you assess magnesium?
- serum Mg (not good measure of total body levels).
- Red cell Mg
- 24 hour urine excretion
- Mg retention test (give load then assess 24 hour urine)
What are the symptoms of hypomagnesaemia?
Weakness and fatigue Fasiculations/cramps Tetany Numbness-paresthesia Seizures Arrhythmias
What are the causes of hypomagnesamia?
- decreased dietary intake
GI malabsorption
Endocrine - hyperaldosteronism, DM, SIADH - Renal loss - congenital, acquired or drug-induced.
Drug induced include, aminoglycosides, amphotericin B
What are the treatment of hypomagnesamia?
Oral or IV administration of Mg
What can cause hypermagnesaemia?
In advanced CKD the compensatory mechanisms start to become inadequate and hypermagnesaemia may develop.
Excessive oral administration of magnesum salts or magnesium containing drugs.
Iatrogenic
Where is the majority of K+?
Intracellular - maintained by the Na/K pump.
Most of it comes from diet.
How is potassium homeostasis maintained?
Most taken in via the diet and most excreted via the kidneys.
In CKD then less is excreted via the kidneys and more is excreted via the faeces.
What happens to the K+ in hyperglycaemia or DKA?
The glucose gets pushed into the cells and the K+ gets pushed out of the cells = hyperkalaemia.
Acidosis can also drive the efflux of K+ and alkalosis wiil drive influx of potassium.
How is potassium reabsorbed from the nephron?
About 60% from the proximal convoluted tubule
- Na/K ATPase bring K= into the lumen of the nephron but then the K+ is reabsporbed paracellularly.
30% from the thick ascending limb.
- ROMK channel bringing potassium into the lumen and then the Na/K/Cl channel bringing it back into the cell
Variable amount from the collecting ducts.
- regulated by aldosterone, which is produced in response to Ang II in hypotension.
What are the symptoms of hypokalaemia?
<3.5 mmol/l
- muscle weakness
- paralysis
- cardiac conduction abnormalities
- cramps
- constipation
How is potassium lost?
Renal
- hyperaldosteronism
- licorice
- diuretics
- renal tubular acidosis
Gut
- vomiting
- diarrhoea
- laxatives
- ileostomy
What are some diuretics that caiuse loose of potassium and where do they act?
Mannitol in the proximal convoluted tubule
Frusemide - thick ascending limb
Metollzone - distal concoluted tubule
Spironolactone and amiloride that act on the collecting duct.
How do you treat hypokalaemia?
Treat the underlying problem/
Use oral for mild losses
Use IV for severe losses.
What are the symptoms of hyperkalaemia?
Fatigue or weakness Paraesthesia Nausia or vomiting Dyspnoea Palpitations
Causes arrhythmias - peak T waves, prolonging of the P interval and widening of the qrs. Can develop of VF and cardiac arrest.
What is pseudohyperkalaemia?
Only in lab tests, if the blood samples are left standing for too long the cells can break down releasing the K+.
What are the causes of hyperkalaemia?
Increased intake.
Disruption of cell intake
- beta blockers
- acidosis
- rhabdomyalsis
Decreased excretion
- renal failure
- hypoaldosteronism
- ACEi/ARB
- other drugs
Addison’s disease - decreased production of aldosterone and cortisol - low blood pressure, high potassium - causes lethargy and weakness - hyperpigmentation
What is the treatment of hyperkalaemia?
Stabilize the action potentials - can do this with IV calcium (lasts 30 minutes) Push K into cells reduce K absorption Increase elimination Fix underlying problem.
Beta agonists (salbutamol) - this will push K intracellularly. (lasts several hours)
Insulin will also push K intracellularly - also need to give with dexterose.
Treat the acidosis - oral bicarbonate.
Reduce K absorption through GI. By giving Ca/K exchangers.
Increase elimination - K+ losing diuretic or dialysis
What is chronic kidney disease mineral and bone disorder?
The kidney retains phosphate. Low calcium causing hyperparathyroidism.
The low calcium is caused by impaired vitamin D metabolism in the kidney, which is required for Ca and Mg intestinal absorption.
Need to reduce dietary phosphate.
Phosphate binders (calcium carboxylase)
Review medications that may contribute to the hyperkalaemia - such as ACEi and ARB
Restrict dietary potassium
What is haemodialysis?
Blood removed put through a machine and cleaned and then put back in.
4-5 hours 3 x per week.
Peritoneal dialysis is another option
What is nephrotic syndrome?
Nephrotic syndrome
- high proteinuria - caused by damage to the basement membrane of the bowmans capsule. No RBCs because the blood vessels are intact.
Causes the serum albumin to be low causing oedema.
What is nephritic syndrome?
Damage to the blood vessels causing an increase of protein and blood in the urine. Causes hypertension and peripheral oedema.
What is rapidly progressing glomerulonephritis?
Rapidly deteriorating renal function and crescents on biopsy.
Can be caused by an Ab that targets the basement membrane or an immune complex
What are cresents in the glomerulus?
They are a sign of glomerulonephritis.
It is a non-specific response to injury of the capillary wall. Physcial gaps appear in the filtration barrier (endothelium, basement membrane and podocyte barrier). This allws RBCs, WBCs and plasma proteins to enter into the bowmans space.
The contents of bowmans space can enter the interstitium, contributing to periglomerular inflammation.
This causes the proliferation of cells in the bowmans space that can cause fibrosis.
The creasents can be cellular or fibrotic. Fibrotic is not reversible.
The degree of cresent formation is associated with the degree of glomerulonephritis.
What is Goodpasture’s disease?
Autoantibody against a type of collagen that is found in both the glomerulous and in the lungs.
It causes haemoptysis and haematuria glomerulonephritis.
Treat with prednisone, cyclophosphamide and give plasma exchange (remove plasma and replace). Dialysis
What are the 5 key m ages about hypertesnion?
1) it is common
2) it is the major cause of morbidity and mortality
3) salt restriction is important
4) long-acting diuretics are the cornerstone of therapy
5) treat using complementary multi-drug therapy and lifestyle changes.
How do you treat modest hypertension?
With monotherapy.
Age <55 years then ACEi
>55 years = diuretics
Social advice
Optimise drug dose - most patients need multiple drugs
What is resistant hypertension?
When the blood pressure is not at target levels despite optimal dose of three complimentary drugs, one of which is a diuretic.
Usually caused by suboptimal doses, or non-complementary drugs, non-compliance, competing drugs (NSAIDS, sodium), white coat hypertension or secondary HT
Secondary causes - endocrine or renal
What is chronic kidney disease determined by?
The cause, GFR and albuminuria
What is end stage kidney disease?
End stage renal failure is insufficient kidney function to keep patients feeling well.
What is glomerulonephritis?
Acute inflammation of the kidney, typically caused by an immune response
Can present as nephrotic syndrome, nephritic syndrome, rapidly progressing GN, asymptomatic urine abnormalities, AKI or CKD
