Chronic Kidney Disease & RRT Flashcards
define CKD
the presence of kidney damage, manifested by abnormal albumin excretion or decreased kidney function, quantified by measured or estimated GFR that persists for more than three months
is CKD reversible or irreversible
irreversible
- renal tissue replaced by extracellular matrix in response to damage
how is CKD measured
by estimated GFR (eGFR)
how is CKD staged
what is the treatment for proteinuria
ACE inhibitors or ARb
decrease hydrostatic pressure pushing protein through
what are the primary causes of CKD
- polycystic kidney disease
- ATN
- recurrent pyelonephritis
- Chronic glomerulonephritis
what are the secondary causes of CKD (4)
- diabetes mellitus
- HTN
- renovascular disease
- autoimmune
80-85% of CKD patients are hypertensive, how is this managed
-Anti-hypertensives
-Diuretics
-Fluid restriction
explain why diabetes can result in hyperfiltration and eventually damage to capillaries (CKD)
- coupled glucose and Na+ reabsorption in PCT so less Na+ in tubule as more glucose being absorbed
- this means macula densa cells low Na+ in DCT and activate RAAS
- renin and aldosterone released increasing BP
-
hyperfiltration then occurs which damages capillaries over time
small amounts of protein will be found in urine
what are some risk factors for CKD
- type 2 diabetes: damage to blood vessels due to activation of RAAS (hyperfiltration of RAAS)
- hypertension: more pressure on glomerulus, too much for regulatory mechanisms to control
- renovascular disease: narrowing of arteries supplying kidneys
describe the gross pathology seen in CKD
severe atrophy of medulla and cortex of kidney with the collecting system mostly spared
how is diabetes monitored in a pt w CKD
fasting plasma glucose
why is HbA1C not used to monitor diabetes in pt w CKD
in CKD patients, EPO is not produced so patient may be anaemic
what are the complications of CKD
- anaema: due to lack of EPO production
- CKD bone mineral disease
- hypertension secondary to chronic intravascular volume overload
- accelerated atherosclerosis/vascular disease
- metabolic acidosis
- CVD - No.1 cause of mortality
why can you not just give EPO replacements in CKD
need iron in order for EPO to make RBC
EPO = builder
iron = building blocks
which diuretic is the most appropriate to treat fluid overload secondary to CDK stage 4
loop diuretic
inhibits Na+K+Cl- co transporter
why do patients often develop anaemia as a result of CKD
- kidney disease: accumulation of uremic toxins e.g. IS, PCS
- decreased EPO
- decreased erythropoiesis in bone marrow
- decreased RBC production = anaemia
why do patients with CKD often develop bone mineral disease and hence non bone calcification
- reduced kidney function means increased plasma PO4- due to less excretion
- reduced kidney function also means it is unable to activate vitamin D leading to reduced absorption of calcium from gut (low plasma Ca2+)
- reduction in plasma Ca2+ triggers release of PTH in from parathyroid gland which increases bone resorption and reduces excretion of PO4-
- large excess of PO4- leads to deposits of calcium phospahate e.g. in blood vessels and joints
how does CKD affect the 4 functions of the kidneys (REEM)
- regulatory
- cannot control acid/base balance –> acidosis
- cannot control fluid balance –> fluid overload
- cannot control PO4 levels –> calcification - excretory
- conc of urea, Cr, PO4 inc in blood –> uraemia - endocrine
- not able to produce EPO or activated vitamin D - metabolism
- reabsorption of glucose
- drug excretion
a patient has the following complications associated with CKD:
- anaemia
- hypocalcaemia
- hyperphosphatemia
- hyperparathyroidism
- hypertension
how would these conditions be managed
- hypertension –ACEI or ARB, 𝛽-blocker or calcium channel blocker
- anaemia –If iron deficient then IV iron usually administered. Once iron replete, he should be commenced on recombinant erythropoietin
- hyperphosphatemia –dietary advice and phosphate binders
- hypocalcaemia/hyperparathyroidism –provide vitamin D. This will reduce PTH secretion, correct hypocalcaemia
- Management of traditional vascular risk factors
Aim for Hb 100-120
what is end stage renal failure
when death likely without renal replacement
- eGFR < 15
when is renal replacement therapy indicated (RRT)
- Required when renal function declines to a level no longer adequate to support health
- Usually when eGFR 8-10
what are the 3 types of RRT
*Haemodialysis
*Peritoneal dialysis
*Renal transplant
describe haemodialysis
- using special filters to remove waste that the kidneys can no longer do on their own
- using mechanisms of diffusion, osmosis and ultrafiltration so that ‘clean blood’ is returned to body
- The dialysis machine pumps blood from the patient, through disposable tubing, through a dialyser, or artificial kidney, and back into the patient. Waste solute, salt and excess fluid is removed from the blood as it passes through the dialyser
what are the pros and cons of haemodialysis
pros
- less responsibility
- days off
- proven effective long term
cons
- Dialysis access needs to be secured
* Infection/Bacteraemia
* Haemodynamic instability
* Reactions to dialysers
* Haematomas/risk of bleeding
* Muscle cramps
* Anaemia due to clotted lines/Haemolysis
* AVF steal syndrome
* SVCO from central lines
describe peritoneal dialysis
- uses lining of abdomen (peritoneal membrane) to filter blood,
- catheter in peritoneum surgically placed
- Solutes (electrolytes, urea, creatinine) move from the patient’s blood, across the peritoneal membrane, down the concentration gradient into the dialysate fluid
what are the pros and cons of peritoneal dialysis
pros
- continously at home = independence
- less fluid/food restrictions
- easy to travel
- renal function may be better preserved intially
cons
- frequent daily exchanges/overnight
- Unsuitable in patients with stoma/previous surgery
* Risk of infection (PD peritonitis)
describe polycystic kidney disease
- Accounts for 8-10% of CKD
- Most common inherited nephropathy
- Presentation at 30-40 years of age with complications of hypertension, acute loin pain and/or haematuria or bilateral palpable kidney
- Cysts develop **anywhere **in the kidney. They compress the surrounding parenchyma and impair renal function
- Autosomal dominant form affects 1 in 500 to 1000
- Autosomal recessive affects 1 in 20,000 to 40,000
describe the macroscopic appearance of PKD
kidneys are large with yellow fluid filled cysts, replacing the parenchyma
- haemorrhage into cysts can occur
describe the microscopic appearance of PKD
cysts lined by cuboidal epithelium
what will an ultrasound or CT of PKD show
bilateral enlarged kidneys w multiple cysts
describe autosomal dominant PKD and its treatment
- Morbidity and mortality are often the result of hypertension, for example, myocardial infarction and cerebrovascular disease
- Condition also leads to progressive CKD
- Treatment involves controlling BP
- Dialysis and renal transplant are needed if endstage renal failure develops
what are some of the clinical manifestations of uraemia
brain & CNS
- stroke
- impaired cognition
- anxiet/depression
heart
- heart failure
- palpitations
body fluid
- leg/facial swelling
- high BP
- shortness of breath
digestion
- nausea
- vomiting
- malnutrition
- diarrhoea
skin
- dry skin: pruritus
- brittle nails
why is the basement membrane of the glomerulus damaged in diabetic neuropathy
high blood pressure (which is caused by hyperfiltration/ renal hypertension)
why does hyperfiltration/ renal hypertension happen in diabetic neuropathy
hyperglycemia
as CKD progresses, what are its clinical features (5)
- Electrolyte disturbances
- Fluid overload
- Metabolic acidosis
- Uraemic pericarditis
- Uraemic encephalopathy
what are the 5 aspects of managing CKD
- treat underlying disease
- reduce CVS risk
- reduce progression of CKD
- prevent or treat complications of CKD
- plan for the future
how is the underlying disease treated in CKD
- Treat and monitor diabetic control
- Treat hypertension
- Treat infections promptly
- Tolvaptan if meets criteria for ADPKD
- Immunosuppression for GN if appropriate
how is cardiovascular risk reduced in CKD
- Start on statin
- Control BP
- Improve control of diabetes
- Advise weight loss
- Advise exercise
- STOP SMOKING
how is disease progression reduced in CKD
- reduce proteinuria - ACEi/ARB
- monitor blood tests
- control BP
most diabetic patients with CKD will undergo screening for diabetic nephropathy - what evidence are you looking for
- Raised Urine Albumin: Creatinine Ratio/PCR
- Evidence of long-standing/poorly controlled DM
- Evidence of other microvascular disease
what is hypertensive nephropathy
chronic raised BP causing nephrosclerosis
what investigations are indicated to identify if primary or secondary HTN (5)
- 24 hour Urinary metanephrines (Phaeochromocytoma)
- Aldosterone: Renin ratio (Primary aldosteronism)
- Cortisol & Dexamethasone suppression test (Cushing’s syndrome)
- TSH (hyperthyroidism)
- MRA (Renal artery stenosis)
what can cause anemia in CKD
- Decreased production of erythropoietin from the kidney
- reduced absorption of Fe
- Absolute iron deficiency (poor absorption and malnutrition)
- Functional iron deficiency (inflammation, infection)
- Blood loss
- Shortened Red Blood Cell survival
- Bone marrow suppression from uraemia
- Medication induced
- Deficiency of Vit B12 and folate
what are blood results of CKD
- increased ALP & PTH
- increased phosphate
- decreased serum Ca2+ & vitamin D
what are the 3 types of peritoneal dialysis
- automated
- continuous ambulatory
- assisted automated
describe features of automated PD
- Carried out with an automated cycler machine performed at night
- 10-12L usually exchanged, over 8-10 hours
- Lifestyle advantages – Leaves the daytime free
describe features of continous ambulatory PD
- Usually consisting of 4-5 dialysis exchanges per day (usually 2 litres each)
- Exchanges are performed at regular intervals throughout the day, with a long overnight dwell
when is active conservative management considered
Decision made after discussion with patient and family members – often after multiple clinic visits and after patient is fully informed of risks & benefits of each mode of therapy
Evidence suggests that if
* Age >80 OR
* WHO performance score of 3 or more
…then RRT offers no survival benefit Often these patients may be unsuitable for or choose to not have invasive therapy such as PD/HD/Transplantation
how is an osmotic gradient created in peritoneal dialysis
Osmotic gradient is created by high concentration of glucose (occasionally amino acid or glucose polymer solutions are used) in the dialysate fluid, which removes water from the patient
what are extra-renal manifestations of ADPKD
- liver cysts (most common) - may cause hepatomegaly
- berry aneurysms: rupture can cause subarachnoid haemorrhage
- cvs: mitral valve prolapse, aortic dissection
what type of anemia is present in CKD
normochromic normocytic anaemia
- becomes apparent when eGFR < 35ml/min
what does anaemia in CKD predispose a patient to
left ventricular hypertrophy - x3 increase in mortality in renal patients
how does reduced absorption of Fe lead to anaemia in CKD
- in CKD there are raised hepcidin levels (acute phase reactant) due to inflammation and reduced renal clearance
- leads to decreased Fe absorption from gut and impaired release of stored Fe from macrophages and hepatocytes
- reduced Fe available for erythropoiesis
what are some of the clinical manifestation of bone disease as a result of CKD
- osteitis fibrosa cystica (hyperparathyroid bone disease)
- adynamic
- osteomalacia due to low vitamin D
- osteosclerosis
what are the complications of peritoneal dialysis
- peritonitis
- sclerosing peritonitis
what procedure do patients need to undergo prior to starting dialysis
AV fistual at least 8 weeks before treatment
what are complications of haemodialysis
- infection
- endocarditis
- stenosis at site
- hypotension
- arrhythmia
what is the most common cause of peritonitis secondary to peritoneal dialysis
Staphylococcus epidermidis is a common cause due to its ability to form biofilms on dialysis catheters
