Lecture 19: Clinical Problem Solving: Kidney Failure Flashcards
What is kidney failure?
Reduction in GFR (Glomerular Filtration Rate)
- High potassium (poor filtration, therefore not peeing out K+)
- Uraemia
- High creatinine (?)
- Oliguria (not passing much urine, may or may not happen)
What do you want to know about a patient?
- History (symptoms)
2. Examination (signs)
Examples of History taking
- Pass urine –> at night?
- Breathless
- Vomitted blood?
- Abdominal pain
- Diabetes –> kidneys involved/damaged –> any medication
- Familial inheritable diseases
JVP measurement as part of Examination
Look at patient ar 45 degrees. Internal Jugular in neck
- Check how many cm pulsation of JVP is above the sternal notch
Normal :1-2cm
If had to lie patient flat in order to get JVP –> -ve
If could see JV pulsating at ear level –> +ve –> fluid overload/congestive HF
- Linked to low BP (e.g. 90/60)
Patient Signs from Examination:
- Afebrile, Looks unwell. BP 90/60, Dry skin, Chest clear, JVP: 0cm, increased creatinine levels, Normal/slightly dropped Hb levels, Normal Calcium, Increased Potassium
Acute:
- history of diarrhea and vomiting + dehydrated
= Pre-renal
Role of Blood Tests
Dont tell you whether it is Acute or Chronic Kidney Failure
- Just that it is Kidney Failure (LOW eGFR)
What other blood tests may help distinguish whether it is acute or chronic kidney failure?
HAEMOGLOBIN test (anaemia)
- elevated ESR (in KF)
- Liver function tests are irrelevant, and Calcium and phosphate levels dont help distinguish
What are Hb levels relevant to distinguishing b/w acute or chronic kidney failure?
RBC life = 120 days –> if EPO levels decrease due to KF will take a long time (chronic) to show and hence become anaemic
Therefore slightly low Hb levels = Acute KF
Very low Hb levels = Chronic KF –> as KF (hence decreased EPO production) must have lasted 120 days to show anaemia
Cycle to produce low Hb levels
Kidney functions:
- Kidney’s get rid of lfuid and electrolytes
- Produce EPO erythropoietin
- Alpha-hydroxylate Vit D (storage form –> active form –> so can absorb Vit D from bone)
Acute Renal Failure
Acute deterioration of kidney function over a short period of time
Usually reversible
Often associated with other illnesses
- diarrohea and vom. –> dehydration –> affects kidney
Pre-renal KF
Due to decreased perfusion of kidneys
Generally low BP (due to low vol.)
- Bleeding
- Sepsis (cytokines –> vasiodilation –> decreased BP)
- Dehydration
- HF ( no heart pumping –> cardiogenic shock –> decreased BP)
Some progress to become intrinsic renal damage (Acute Tubular necrosis)
Renal KF
Mainly ATN (Acute Tubular Necrosis) --> due to pre-renal that wastnt treated early enough - Acute= Toxins. Tubular= Renal
Causes of Renal KF
Aminoglycosides: antibiotics for gram -ve infections
Contrast: CT, angiograms
NSAIDS: neurophen w/o hydration
Rhabdomyolysis:
- acute muscle breakdown –> toxin release –> acute kidney failure
- trauma
-venom/toxin (crack/cocaine/heroine/ bee stings)
Other causes of intrinsic renal failure (not ATN)
RPGN (Rapid Progressive GlomeruloNephritis)
- Rapid acute renal failure (from glomerulus inflammation)
- Cresents in glomeruli on biopsy
- Red cells and cast cells in urine (SLE/Lupis, vasculitis, post-Streptococcal GN)
What is the best test for Post-Renal AKI?
Renal Ultrasound
- can always palpate bladder, but only useful if obstruction is at bladder outlet (enlarged prostate)
- not urine volume or looking for haematuria
- can only palpate a polycystic kidney
Treatment for having an enlarged bladder
Hydronephrosis –> needs draining
Hypervolemia
Fluid overload
- Edema (swelling) - particularly feet and ankles
- 3kg of fluid per leg. press hard on shin bone - Difficulty breathing while lying down (orthopnea - difficulty breathing when lying flat in bed)
- Crackles on auscultation (when breathing)
- High BP
- Irritated cough
- Jugular Vein distension
- Shortness of breath (dyspnea)
- Strong, rapid pulse (tachycardia)
Meaning of 6ml/min
6% of normal kidney function
Presentation of Chronic KF
Most people wont have an acute presentation until their renal function is really bad
GFR 30/40 = no signs/symptoms
GFR Less 15 = some KF symptoms (Uraemia)
Uraemia
Nausea, vomiting, cold intolerance, itchiness, breathlessness
Patient Signs from Examination:
- 10 days of vomitting, unwell, past history, diabetes 15 years, hypertension, very anaemic, no history of bleeding
Chronic KD
Signs of CKD
- (protein) malnutrition : Wasted, weight loss, look unwell
- cant eat as feel to sick and nauseated - Fluid overload
- High BP, oedema (swelling), pulmonary oedema - Rash (uremic toxin build up in skin/ hyperphosphatemia makes itchy)
- Pericardial Rub ( inflammation b/w pleural layers –> fluid in pericardium –> crunchy noise –> pleural rub heard when breathing)
Blood rests to help distinguish b/w acute or chronic KF
Most blood tests that are abnormal in KF are abnormal just becuase the kidney doesnt work properly
- High potassium, urea, creatinine and phosphate
Same for both acute and chronic
BUT Hb is LOW in chronic Renal Failure (average RBC lifespan of 120 day)
Diabetes rates
Main cause for CKD
Increased risk proportionately in Maori, pacifica and asian populations (23.5%)
Type II common in NZ
For every diagnosed diabetic there is another undiagnosed (therefore rates are actually high than expected)
What tests might be helpful to confirm diagnosis?
- Kidney size (normal 10-11cm) (see on US)
2. Presence of obstruction
State of Kidney in CRD re tests to confirm diagnosis
- Small (6cm) kidney size
- check for post-acute kidney failure
Main causes of CKD
- Diabetes (main reason)
- Hypertension (Increased BP) 20%
- Glomerular disease 20%
Renal Ultrasound
Normal Kidney size 10-11cm
Kidneys less than 8cm highly likely to be due to CRF
What is the best treatment to treat deterioration of CKD?
TREAT BP
- treating the anaemia wil help the patient feel better, and slows the progression of chronic kidney disaese
- HbA1c <7.0 - glycemic control- helps slow development into neuropathy. NO help if you ALREADY have CKD
- Can give dialysis to decreased BP, but will just Delay death, wont prevent/cure end stage Kidney failure/death
BP control
BP control (BP under 130) is the best treatment to help prevent patients from getting worsened renal function High Bp = massively increased risk of developing end stage kidney failure Normal (<120/80) or optimal (<110/70) = being is either of these BP ranges both leads to a massively lower risk of develping end-stage renal fialure
What best BP treatment for CKD works the best?
ACE inhibitors/ Receptor blockers
Note: most people require multiple BP lowering pills, as the key treatment is having BP control
- Beta blockers, Diuretics
Why are ACE inhibitors/Receptor blockers the best treatment for High BP in CKD?
RAAS 1. slat and h2o control
RAAS 2. vasoconstriction and angiotensin
3. Preferentially vasodilates the Efferent arteriole –> decreased BP in glomeruli –> decreased ongoing damage to glomerulus itself due to the High BP
Where do ACE inhibitors and ACE receptor blockers act?
ACE inhibitors: no AI –ACE–> AII
ACE Receptor Blockers: no AII binding to AI1 receptor
What happens when you decrease the BP in the glomerulus?
Decreased damage to glomerulus itself –> decreased ongoing structural damage
- done by ACE inhibitors by both RAAS steps 1 and 2, but also by step 3 Preferentially vasodilating the efferent arteriole in the glomerulus
