Transcript renal case - Ipswich-Year2-Med-PBL-Gp-2

Week 26
Additional Renal Case 1
Shannon and Skye
Trigger
Donald is a 68 year-old man who is admitted
to hospital via the Emergency Department
one day, following a myocardial infarction.
Subsequent investigation reveals that his
eGFR is 42 mL/min/1.73m2. He comes to
see you after his discharge, to discuss his
kidney problem.
Q.1 What stage of Chronic Kidney
Disease (CKD) does this represent?
Q.1 What stage of Chronic Kidney
Disease (CKD) does this represent?
• Stage 3 CKD – moderate decreased
kidney function
• No way to
know this
other than
memorising
/referring to
this
table…..
Q.2. What modifiable risk factors for CKD
would you specifically seek in order to
address them and slow progress to
End Stage Renal Disease (ESRD)?
Modifiable risk factors for CKD
Modifiable risk factors: the 4 biggies
• smoking
• Diabetes (blood glucose)
• high blood pressure
• Obesity
Others (?)
•
Cardiovascular risk reduction:
–
–
Lipids
Other lifestyle modification: physical activity, nutrition, alcohol
•
Medication: nephrotoxic drugs, drug dosages appropriate for level of kidney function
•
Non-modifiable risk factors:
–
–
–
age over 50 years
family history of kidney disease
Aboriginal or Torres Strait Islander heritage
Q.3. Briefly outline the key points in the relationship between kidney
and cardiovascular disease.
Q.3. Briefly outline the key points in
the relationship between kidney and
cardiovascular disease.
• The presence of CKD is one of the most potent
known risk factors for cardiovascular disease
• Individuals with CKD have a 10–20 fold greater
risk of cardiac death than age and sex matched
controls without CKD
• People with CKD are at least 20 times more
likely to die from cardiovascular disease than
survive to need dialysis or a transplant
Up-to-date
• Chronic kidney disease (CKD) alone is an independent
risk factor for the development of coronary artery
disease, and for more severe coronary heart disease
(CHD)
• CKD is also associated with an adverse effect on
prognosis from cardiovascular disease. This includes
increased mortality after an acute coronary syndrome
and after percutaneous coronary intervention (PCI) with
or without stenting
• In addition, patients with CKD are more likely to present
with atypical symptoms, which may delay diagnosis
and adversely affect outcomes
• MECHANISM BEHIND RELATIONSHIP ? UNCLEAR
Q.4. Briefly outline the key points in your
clinical action plan for this man.
Q.4. Briefly outline the key points
in your clinical action plan for
this man.
Based on modification of future cardiovascular risk.
•
•
•
•
Recommended modalities include:
Statin therapy
Control of hypertension to below target of 140/90 mmHg
(use ACEI/ ARB if proteinuric to below target of 130/80
mmHg).
Low-dose Aspirin therapy
Smoking cessation, maintenance of ideal body weight,
tight glycaemic control etc
• Moniter eGFR three monthly
• Avoid nephrotoxic drugs, ensure drug doses appropriate
• Monitor/address common complications
Address the causes of CKD
Treatment of reversible causes of renal dysfunction
•
•
•
Decreased renal perfusion: Hypovolemia (V&D, diuretic use, bleeding),
hypotension (MI or pericardial disease), sepsis, and NSAIDS, ACEI and
diuretics etc that lower GFR.
Ie. Hypovolemia may actually be present in CKD because diseased kidneys
can’t resorb Na as well as they should – fluid replacement should be trialed
if clinically dehydrated.
Administration of nephrotoxic drugs: eg. Aminoglycosides, NSAIDS,
vancomycin
Urinary tract obstruction: Renal ultrasonography is often performed to
exclude urinary tract obstruction in patients with an unexplained elevation in
the serum creatinine.
Preventing or slowing the progression of renal disease
• Glomerulosclerosis: Due to HTN in glomerulus, as well as metabolic
acidosis and hyperlipidemia – ACEI/ ARB will slow/ prevent progression of
CKD. (Statin therapy and smoking cessation helps too)
Treatment of the complications
of renal dysfunction
•
•
•
•
Volume overload: Tx with sodium restriction and diuretic therapy
Hyperkalemia: Tx with Calcium chloride/ gluconate to protect heart, then lower serum
K+ with glucose/ insulin, also use salbutamol and sodium bicarbonate acutely then
institute potassium binding resins.
Metabolic acidosis: Bicarbonate supplementation may slow the progression of both
chronic kidney disease and resultant bone disease.
Hyperphosphatemia: Reduction in ability to filter phosphate begins early in renal
disease, and it’s affect on serum calcium causes PTH to be secreted – resulting in
renal osteodystrophy.
–
•
Tx with dietary phosphate restriction and oral phosphate binders (when GFR <30ml/min) eg.
Calcum carbonate, Sevelamer, Lanthanum, Aluminium hydroxide (not good), Calcium citrate
etc. taken with meals.
Anaemia: Normocytic normochromic, due to reduced EPO production by the kidney
Tx with recombinant erythropoietin or darbepoetin alfa
Q. 5. Why is it important to screen at-risk persons for CKD?
Q. 5. Why is it important to
screen at-risk persons for CKD?
• Therapeutic interventions implemented
early in the course of CKD are effective in
slowing or preventing the progression
toward ESRD and its associated
complications
Q. 6 What symptoms of uremia may
occur in ESRD?
Q. 6 What symptoms of uremia
may occur in ESRD?
•
Malnutrition — due to anorexia, decreased intestinal absorption and digestion, A low
plasma concentration of albumin and/or creatinine (which varies with muscle mass as
well as GFR) may be indicative.
•
Uremic bleeding — Due to prolongation of the bleeding time, due primarily to impaired
platelet function. Not normally treated unless patient is actively bleeding or about to
undergo surgery etc
•
Pericarditis — Fever, pleuritic chest pain, and a pericardial friction rub are the major
presentations of uremic pericarditis, although other causes should be ruled out.
•
Uremic neuropathy — Dysfunction of the central and peripheral nervous system,
including encephalopathy (impaired mental status progressing if untreated to seizures
and coma), polyneuropathy, and mononeuropathy are important complications of endstage renal disease. They have become much less common because of the current
tendency to earlier initiation of dialysis.
•
Thyroid dysfunction — the kidney normally plays an important role in the metabolism,
degradation, and excretion of several thyroid hormones. It is not surprising therefore that
impairment in kidney function leads to disturbed thyroid physiology.
Other signs and symptoms
include:
– Decreased sense of smell and taste
– Cramps
– Restless legs
– Sleep disturbances
– hyperreflexia and Babinski reflex present
– uremic fetor
– nausea/vomiting
– Amenorrhea and sexual dysfunction
– Reduced body temperature