CKD Flashcards
What is the definition of CKD?
Sustained and irreversible disease in GFR
can be any of:
- <60mL /min/1.73m2 for at least 3 months
- persistent haematuria,
- proteinuria
- or structural abnormalities of the kidney
NB: there are multiple equations used to calculate CKD (MDRD, CKD-EPI, Cockcroft-Gault)
What GFR levels is end stage renal disease?
GFR <15
aka need for RRT
most common causes include DM, glomerulonephritis, HTN
What conditions are associated with chronic kidney disease?
- HTN
- CVS complications (RAAS)
- anaemia (EPO)
- mineral and bone disorders (activation of vitamin D)
what patient groups experience stable vs progressive loss of kidney function?
- Elderly: CKD more prevalent in this population, ~30% patients >65yrs have stable disease
- Young: CKD less common, but patients typically experience progressive loss of kidney function
How does the presence of CKD stage 1-3 differ from stages 4&5?
-
Stages 1-3 (GFR > 30mL/min)
- frequently asymptomatic e.g. via screening of at-risk patients
-
Stages 4-5 (GFR < 30mL/min)
- endocrine / metabolic / water / electrolyte disturbances clinically manifest
NB: CKD Can co-exist with other things e.g. nephrotic syndrome
Which stage is GFR between 60-89?
Stage 2
What is normal GFR?
~120
What stage is GFR ~90?
Stage 1 CKD
What symptoms / clinical findings may you expect if GFR ~90 e.g. stage 1 disease?
Normal kidney function
but urine findings or structural abnormalities or genetic trait point to kidney disease
What are the complications of CKD stage 1?
none
(90+ GFR - Normal kidney function but urine findings or structural abnormalities or genetic trait point to kidney disease)
What is the Rx of GFR ~90+?
Stage 1 kidney disease, Rx:
- –> observation,
- –> control of blood pressure
What symptoms clinical findings may you have with GFR 60-89?
- GFR 60-89 = stage 2 kidney diseaase
- –> mildly reduced kidney function
- other findings like for stage 1, that point to kidney disease AKA - normal kidney function but urine findings or structural abnormalities or genetic trait poinnt to kidney disease
What complications may arise if GFR is 60-89 (stage 2 CKD)?
Increased CVD
What is the Rx of GFR is 60-89 (stage 2 CKD)?
- Observation
- control of BP
- control of RF’s (as increased CVD risk @ stage 2)
What stage is GFR 45-59?
3A
What stage is GFR 30-44?
3B
What symptoms / clinical findings do you get with stage 3A (GFR 45-59) and 3B (GFR 30-44)?
stage 3A (GFR 45-59) and 3B (GFR 30-44) => moderately reduced kidney function
What complications do you get with stage 3A (GFR 45-59) and 3B (GFR 30-44)?
- increased CVD;
- bone disease - high PTH (from kidneys not converting to ative vit D to absorb Ca2+)
How do you Rx stage 3A (GFR 45-59) and 3B (GFR 30-44)?
- Observation,
- & control of blood pressure
- & risk factors
- –> (Increased CVD; bone disease - high PTH)
A patient has GFR 15-29 what stage kidney disease is this?
Stage 4
What complication may happen with a gfr of 15-29?
e.g. Stage 4
- Increased CVD;
- bone disease - low Ca (no vit d) high phosphate
With a GFR of 15-29 what treatment stage planning is needed?
stage 4 GFR need planning/educaate for end stage (whereas stage 3 was observation, control of blood pressure & RFs)
What happens to a patient who has a GFR < 15?
GFR <15 or on diaysis = stage 5 renal disease = very severe or endstage kidney failure
(sometimes called established renal failure)
this is the treatment stage where you need renal replacement therapy
What are the complciations of having a GFR <15?
- increased CVD
- bone diseaes
- pruritus
- bleeding
- malnutrition
What findings are needed to confirm stage 1 or 2 CKD because gfr alone is insufficient?
the definition of CKD = sustained and irreversible decrease in GFR (<60) e.g. stage 2 when you start to get complicatons. or persistent haematuria, proteinuria or structural abnormalities of the kidney so they need to include those in dx:
-
Albuminuria
- (albumin excretion >30 mg/24 hr
- or albumin:creatinine ratio >30 mg/g [>3 mg/mmol]) [raised creatinine 1.5x baseline = AKI]
- Urine sediment abnormalities
- Electrolyte and other abnormalities due to tubular disorders
- Histologic abnormalities
- Structural abnormalities detected by imaging
- History of kidney transplantation in such cases
What pathological manifestation of CKD is salt & fluid restriction, loop diuretic the management for?
the abnormal excretory funciton of the kidney causing fluid retention –> HTN
What pathological manifestation of CKD is managed by low K+ diet and correcting acidosis?
due to the abnormal excretory function of the kidney and potassium retention –> hyperkalaemia (muscle fatigue, weakness, arrhythmias)
[normally aldosterone is na retain and K and H loss)
What pathological manifestation of CKD’s management is a low phosphate diet, phosphate binders?
(phosphate binders = tablets taken just before eating, they bind phosphate in the gut and stop it being absorbed)
due to the abnormal excretory funciton of the kidney you get phosphate retention
–> hyper-phosphataemia
What pathological manifestation of CKD is managed by sodium bicarbonate therapy?
abnormal excretory function –> retention of acid –> metabolic acidosis –> sodium bicarb therapy
What are the pathological manifestations of CKD due to abnormal excretory function and their rx?
- Fluid retention –> HTN –> salt and fluid restriction, loop diuretic
- potasisum retnention –> hyperkalaemia (muscle fatigue, weakness, arrhythmias)
- phosphate retention –> hyperphosphataemia (low phos diet, phos binders)
- retention of acid –> metabolic acidosis –> Na bicarb therapy
NB: renal diet = limit K, phos, salt and dc water too if needed
For what pathological manifestation of CKD do you get rx’d with epotin, iron and ferritin?
due to lack of EPO production –> anaemia –> tiredness and LVH that needs Rx with epotin, iron & ferritin
(EPO is made in the interstitial fibroblast cells around the PCT)
What pathological manifestation of CKD is Rx’d by vit D/calcium supplementation?
the lack of 1,15 vit D production –> hypocalcaemia –> bone pain
rx: vit D/calcium supplementation
What pathological manifestation of CKD is Rx’ed by
Phosphate-binders, vit D/analogues, calcimimetics
1-alpha-calcidiol (1- hydroxylation done by kidney, note 25- hydroxylation first & is in liver)
hypocalcaemia from lack of 1,25 vit D production –> hypocalcaemia –> raised PTH –> #, osteomalacia, osteitis fibrosa
In the pathological manifestations of CKD is the mangagement of ACEi and ARB used for?
the effefct of kidney abnormality on CVS heathl
e.g. RAAS activation –> LVH
needs ACEi or ARB
What kidney abnormality needs BP control <130/80?
the effect of kidney abnormality on CVS health
Microinflammation and HTN (from fluid retention/RAAS)
–> CAD, CHF, arrythmias
What are these SSx of?
- CNS: encephalopathy, fits, twitch or tremor, tiredness
- Peripheral neuropathy, restless leg syndrome
- GI: anorexia (loss of appetite & weight), N&V, colitis, metallic taste, halitosis
- Lungs: pleuritis, pleural effusion
- Heart: pericarditis
- Endocrine: growth retardation, sexual dysfunction, amenorrhoea
- Skin: pruritus, dry skin, ecchymosis, “half-and-half” nails
- PRO-HAEMORRHAGIC - impaired platelet function
Uraemia SSx
- CNS: encephalopathy, fits, twitch or tremor, tiredness
- Peripheral neuropathy, restless leg syndrome
- GI: anorexia (loss of appetite & weight), N&V, colitis, metallic taste, halitosis
- Lungs: pleuritis, pleural effusion
- Heart: pericarditis
- Endocrine: growth retardation, sexual dysfunction, amenorrhoea
- Skin: pruritus, dry skin, ecchymosis, “half-and-half” nails
- PRO-HAEMORRHAGIC - impaired platelet function
What is the pathophysiology of CKD?
primary kidney injury –> nephron loss –> hyperfiltration (compensating for the loss) –> sclerosis of those nephrons –> nephron loss w/ ensuing GFR decline
What problems can cause primary kidney injury in the pathophysiology of CKD?
aka: primary kidney injury –> nephron loss –> hyperfiltration (compensating for the loss) –> sclerosis of those nephrons –> nephron loss w/ ensuing GFR decline
- *Diabetes
-
Glomerulonephritis
- commonly IgA nephropathy,
- also rare disorders e.g. mesangiocapillary GN,
- systemic disorders e.g. SLE, vasculitis
- Hypertension or reno-vascular disease
- Pyelonephritis & reflux nephropathy
In CKD there is increased glomerular capullary pressure that may damage the capillaries, where does this come from?
damage to the capillaries by increased glomerular capillary pressure occurs in hyperfiltration and hypertrophy of residual nephrons*
- primary kidney injury –>
- nephron loss –>
- _*hyperfiltration (residual nephrons compensating for the loss)_ –>
- sclerosis of those hyperfiltering nephrons –>
- nephron loss w/ ensuing GFR decline
What process happens to lose nephrons at a certain point in the pathophysiology of CKD?
aka: primary kidney injury –> nephron loss –> hyperfiltration (compensating for the loss) –> sclerosis of those nephrons –> nephron loss w/ ensuing GFR decline
* at a certain point the remaining nephrons begin a process of irreversible sclerosis & progressive decline in GFR ensues
What other influencing fators are there on CKD pathopgenesis/physiology?
Other influencing factors:
- nephrotoxins (e.g. NSAIDs),
- decreased perfusion (e.g. dehydration, shock),
- proteinuria,
- hyperlipidaemia,
- hyperphosphatemia with calcium phsophate deposition,
- smoking
7.
The aim of Ix in CKD is to determine aetiology and evaluate complications…
What Ix should be done for CKD?
Blood:
- FBC (anaemia), ESR, U&E, glucose,
- low Ca, high phosphate, high ALP, high PTH
Urine:
- dip, MC&S, albumin : creatinine ratio
- significant proteinuria (glomerular disease)
- dysmorphic RBCs, RBC casts (glomerulonephritis)
- Bence Jones (myeloma)
Imaging/invasive:
- US kidney (small in CKD)
- & USS bladder (obstruction)
- Biopsy
What is the management of CKD?
(5x steps)
- Identify & treat reversible causes
- Delaying or halting the progression of CKD
- Manage CVD risk
- Diagnosing and treating the pathologic manifestations of CKD
- Timely planning for long-term renal replacement therapy
The management of CKD involves identifying and treating reversible causes, what is the Rx of this?
Relieve obstruction
avoid nephrotoxins e.g. radiocontrast, NSAIDS, aminoglycosides
The Rx of CKD involved the delaying or halting of the progression of CKD, what is this refering to?
- BP
- even a small drop may save significant renal function
- 2 or 3 anti-hypertensives e.g. ACEIs, angiotensin-II receptor antagonists; salt restriction
The Rx of CKD involved managning the CVD risk, how is this done?
Lifestyle factors
BP, lipid & glycaemic control
The Rx of CKD involves diagnosing and treating the pathologic manifestations of CKD.
What does this involve?
- Treat anaemia
- B12, folic acid, iron (IV can be useful), EPO stimulation
- If suspect red cell aplasia (anti-EPO antibodies) get haematology help
- Treat restless legs/cramps
- –> made worse by/caused by anaemia, low iron or high calcium; uraemia also gives restless leg
- –> check ferrtin, clonazepam or gabapentin may help, quinine helps with cramps
- Treat mineral & bone disorders
- Vit D analogues, phosphate binders, Ca supplements
- Treat acidosis
- consider sodium bicarbonate supplements (caution as can raise BP)
- Treat oedema
- furosemide 250mg02g/24h +/- metolazone 5-10mg/24hr PO, fluid & sodium restriction
*
- furosemide 250mg02g/24h +/- metolazone 5-10mg/24hr PO, fluid & sodium restriction
one of the last steps in management of CKD is timely planning for long term renal replacement therapy, what does this involve?
- haemodialysis (complications: hypotension, bleeding, vascular access clot, G+ve blood steam infection)
- Usually begin dialysis when GFR <10mL/min (<15 in diabetics)
- Or when uremic symptoms [pericarditis, peripheral neuropathy/restless let, pruritis, anorexia, N&V}
- peritoneal dialysis (complications: infectious peritonitis)
- renal transplantation (complications: rejection, infection with unusual organisms e.g. CMV, PCP, fungi, delayed graft function (ATN in graft due to ischaemia-reperfusion injury), drug toxicity, malignancy, cardiovascular disease
What are the indications for dialysis?
- refractory metabolic acidosis
- refractory hyper-K+ after 3x rounds of treatment [e.g. insulin dex, salbutamol etc]
- refractory anuria/uraemia (increased blood urea from ammonia)
-
BLAST drugs (can be filtered out body as not bound to any proteins):
- barbiturates,
- lithium,
- alcohol,
- salicylates,
- theophylline’s
Which is more brutal, haemofiltration or haemodialysis?
Why is this used?
Haemofiltration = less brutal than haemodialysis
TF haemofiltration is suitable for much more sick ITU patients
What is the difference between haemodialysis and peritoneal dialysis?
haemodialysis uses an external membrane
peritoneal dialysis uses a peritoneum filter
What are the positives of having haemodialysis e.g. an external membrane?
- HCPs can watch for any problems.
- Meet other people having dialysis - may give you emotional support.
- You don’t have to do it yourself
- Shorter time & fewer days each week
- Home haemodialysis: more flexibility in when, where, and how long you have dialysis
What are the negatives of haemodialysis (external membrane)?
- Site needed – Arterio-venous fistula (adequate blood flow)
- Takes weeks to mature; ideally be fashioned 3-6 months before starting
- Requires regular hospital visits
- 3-5hrs 3x a week PLUS travel
- Feel tired on the day of the treatments.
- Need to be able to cope with cardiovascular strain of huge changes in blood volume
- Home hemodialysis expensive, home moderations etc & these candidates are usually good for transplant!
What are the positives of peritoneal dialysis e.g. peritoneum filter?
- Arguably more freedom than hemodialysis
- At home – no travel to hospital
- On holiday
- While asleep
- You can do it by yourself.
- Not as many food and fluid restrictions
- It doesn’t use needles.
What are the negatives of peritoneal dialysis (uses a peritoneum filter)?
- The process of doing peritoneal dialysis is called an exchange.
- You will usually complete 4 to 6 exchanges every day.
- Requires teaching patient/careers
- The procedure may be hard for some people to do.
- ST lifespan - membrane changes after a few years!
What are the CI’s for peritoneal dialysis?
- Absolute:
- Intra-abdominal adhesions and abdominal wall stoma.
- Relative CI:
- `Obesity, intestinal disease, respiratory disease and hernias are relative contra-indications.
What are the risks of haemodialysis?
- Access-related:
- local infection, endocarditis, osteomyelitis, creation of stenosis, thrombosis or aneurysm.
- Fever: infected central lines.
- Haemodyalysis itself:
- Hypotension (common), cardiac arrhythmias, air embolism.
- Nausea and vomiting, headache, cramps.
- Dialyser reactions:
- anaphylactic reaction to sterilising agents.
- Heparin-induced thrombocytopenia, haemolysis.
- [UFH administered at dialysis time to prevent clotting in blood circuit]
-
Disequilibration syndrome:
- restlessness, headache, tremors, fits and coma.
- Depression.
Rememeber for haemodialysis pt needs to be able to come with CVS strain of huge BV changes
What are the risks of peritoneal dialysis (peritoneum filter)?
- Peritonitis, sclerosing peritonitis.
- Catheter problems:
- infection, blockage, kinking, leaks or slow drainage.
- Constipation, fluid retention, hyperglycaemia, weight gain.
- Hernias
- (incisional, inguinal, umbilical).
- Back pain.
- Malnutrition.
- Depression.
(rememeber peritoneal dialysis has ST lifespan as membrane changes after a few years)
What are these complications of?
- Cardiovascular disease - MI & CVA
- Malnutrition
- Renal bone disease
- Infection
- Malignancy e.g. urothelium tumours
Renal replacement therapy complications
- Cardiovascular disease - MI & CVA
- Malnutrition
- Renal bone disease
- Infection
- Malignancy e.g. urothelium tumours
Name this drug.
used to prevent & control excessive thirst, urination & dehydration caused by injury, surgery, or medical condition ..
= desmopressin!
a chemical that is similar to Antidiuretic Hormone (ADH), a synthetic analogue, which is found naturally in the body - ↑s urine concentration & ↓s urine production.
What are the different uses of oral and intranasal/parenteral formulations of desmopressin?
-
Oral formulations indications:
- Primary nocturnal enuresis in adults
- Vasopressin sensitive diabetes insipidus
- Control of temporary polyuria and polydipsia following head trauma or surgery in the pituitary region.
-
Intranasal and parenteral formulations:
- Spontaneous or trauma-induced bleeds (e.g. hemarthrosis, intramuscular hematoma, mucosal bleeding) in patients with hemophilia A or von Willebrand’s disease Type [clotting disorders, e.g. get blood volume back up]
- Prevent or treat bleeding in patients with uraemia
So overall parenteral/intranasal used for uraemia bleeds or clotting disorder trauma bleeds; oral desmopressin/ synthetic ADH = diabetes insipidus, and enuresis. Also for head/pituitary trauma –> thirst and weeing.
