Renal + Urology High Yield Flashcards
what are Renal stones and their types
AKA renal calculi, urolithiasis and nephrolithiasis
RF
- dehydration
- hypercalciuria, hyperparathyroidism, hypercalcaemia
- cystinuria
- high dietary oxalate + protein diet
- antacids
- renal tubular acidosis
Drug causes
- drugs that promote calcium stones: loop diuretics, steroids, acetazolamide, theophylline
- thiazides can prevent calcium stones (increase distal tubular calcium resorption)
- May be asymptomatic until they irritate or get stuck in the ureters. Usually stuck a 3 junctionsCommonly at vesico-ureteric joint
- Can cause obstruction (AKI) and/or infection (pyelonephritis)
Types
- Calcium Oxalatae - Most common 85% - Radio-opaque on Xray.
- Calcium Phosphate - 10% - Radio-opaque on Xray
- Uric Acid - 5-10%, low pH, product of purine metabolism, cancers?, Radio-lucent
- Struvite 2 -20%, result of urease producing bacteria ( associated with chronic infections) - Radio-opaque
- Cysteine 1%, associated with cystinuria, an autosomal recessive disease - radio-dense
Staghorn Calculus stone forms in the shape of the renal pelvis. Common with Struvite stones where bacteria (from URTI or other infection) converts urine into ammonia. Infection with Proteus mirabilis accounts for 90% of all proteus infection
Presentation of Nephrolithiasis
Renal stones may be asymptomatic and never cause an issue.
When they do it leads to: Renal Colic
Renal Colic
- Unilateral loin to groin pain that can be excruciating (“worse than childbirth”)
- Colicky (fluctuating in severity) as the stone moves and settles
- Nausea or vomiting
Also
There may also be:
- Excessive movements
- Haematuria
- Reduced urine output
- Symptoms of sepsis, if infection is present
Management of Renal Colic
include investigations
- IM Diclofenac - IV paracetamol if NSAID contraindicated
- Alpha Blocker - Tamsulosin - If stone <10mm (smooth muscle relaxation and dilation)
Investigations
- Urine dipstick: checkking for haematauria and Infections
- Serum creatinine and electrolytes: check renal function
- FBC/CRP: looking for Infections
- Non Contrast CT-KUB within 24h of admission, if feverish or solitary kidney then investigate as soon as
- USS used in children and pregnant ladies - low sensitivity
Management of Confirmed Nephrolithiasis in Renal Vs Uretic
after managing renal colic and confirmed using CT-KUB
Shockwave lithotripsy
Ureteroscopy
nephrolithotomy
Renal
- If stone is <5mm = wait & watch
- 5mm-10mm - shockwave lithotripsy
- 10-20 mm shockwave lithotripsy OR ureteroscopy
- > 20 mm percutaneous nephrolithotomy
Uretic
- Stone <10mm Shockwave lithrotripsy + Tamsulosin
- 10-20 mm ureteroscopy
Severe Cases
- Infection presents with stones
- Needs Renal Decompression + abx
- Nephrostomy tube placement, insertion of ureteric catheters and ureteric stent placement.
Lithotripsy contraindicated in pregnancy
Prevention of future Nephrolithiasis occurence
Calcium stones
may be due to hypercalciuria, which is found in up to 5-10% of the general population.
high fluid intake
add lemon juice to drinking water
avoid carbonated drinks
limit salt intake
potassium citrate may be beneficial
thiazides diuretics (increase distal tubular calcium resorption)
Oxalate stones
cholestyramine reduces urinary oxalate secretion
pyridoxine reduces urinary oxalate secretion
Uric acid stones
allopurinol
urinary alkalinization e.g. oral bicarbonate
Acute Kidney Injury Definition (incl. signs + symptoms)
common in acutely unwell patients
RF
- Older age (e.g., above 65 years)
- Sepsis
- Chronic kidney disease
- Heart failure
- Diabetes
- Liver disease
- Cognitive impairment (leading to reduced fluid intake)
- Medications (e.g., NSAIDs, gentamicin, diuretics and ACE inhibitors)
- Radiocontrast agents (e.g., used during CT scans)
- Rise in creatinine of more than 25 micromol/L in 48 hours
- Rise in creatinine of more than 50% in 7 days
- Urine output of less than 0.5 ml/kg/hour over at least 6 hours
Symptoms - often not seen untill diseases progression
- pulmonary and peripheral oedema
- arrhythmias (secondary to changes in potassium and acid-base balance)
- features of uraemia (for example, pericarditis or encephalopathy)
Stage 1: 0.5 ml/kg/hour over at least 6 hours. Creatinine 2x baseline
Stage 2 0.5 ml/kg/hour over at least 12 hours Creatinine up to 3x baseline
Stage 3: 0.3 ml/kg/hour over at least 24h Creatinine more than 3x baseline
Causes of AKI
Divided into 3
Pre-Renal Insufficient blood supply (hypoperfusion) to kidneys reduces the filtration of blood. This may be due to:
- Hydration
- Shock (e.g., sepsis or acute blood loss)
- Heart failure
- Renal Artery stenosis
Renal (Intrinsic diease of kidney)
- Acute tubular necrosis
- Glomerulonephritis
- Acute interstitial nephritis
- Haemolytic uraemic syndrome
- Rhabdomyolysis
- Tumour Lysis Syndrome
Post-Renal causes involve obstruction to the outflow of urine away from the kidney, causing back-pressure into the kidney and reduced kidney function. This is called an obstructive uropathy. Obstruction may be caused by:
- kidney stone in ureter or bladder
- benign prostatic hyperplasia
- external compression of the ureter
- tumours
Management of AKI
Largely Supportive
What are the complications of unresolved AKI
- Stop Drugs with nephrotoxic potential
- Ok to continue with: Paracetamol, warfarin, aspirin (75mg), Clopidogrel, statins, B Blockers.
- Carefully moniotred Fluids
Specialist is reqd for when the cause is unknown or the AKI is severe.
Complications
Fluid overload, heart failure and pulmonary oedema
Hyperkalaemia
Metabolic acidosis
Uraemia (high urea), which can lead to encephalopathy and pericarditis
These indicate haemodialysis
Treating Hyperkalaemia in AKI
to avoid arrhythmias which may potentially be life-threatening
Stabilising Cardiac Membrane
- Calcium Gluconate
Shifting K+ from ECF to ICF
- Combined insulin/dextrose infusion
- Nebulised salbutamol
Removal of potassium from the body
- Calcium resonium (orally or enema)
- Loop diuretics
- Dialysis
When is Renal Replacement Therapy indicated in AKI
Renal replacement therapy (e.g. haemodialysis) is used when a patient is not responding to medical treatment of complications, for example hyperkalaemia, pulmonary oedema, acidosis or uraemia (e.g. pericarditis, encephalopathy).
Differentiating between AKI and CKD
- CKD: Bilateral small kidneys USS.
Except: ADPCKD, diabetic nepthropathy, amyloidosis, HIV - CKD: Hypocalcaemia due to no VitD.
Acute interstitial nephritis
Acute interstitial nephritis accounts for 25% of drug-induced AKI
Causes
Drugs: the most common cause, particularly antibiotics
- penicillin
- rifampicin
- NSAIDs
- allopurinol
- furosemide
Systemic disease: SLE, sarcoidosis, and Sjogren’s syndrome
infection: Hanta virus , staphylococci
Histology: marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules
Symptoms: Fever, Rash, Arthralgia, eosionophila (excess eosinophills), renal impairment, HTN
Ix: sterile pyuria + white cell casts
- RAISED EOSINOPHILS
Drugs with nephrotoxic potential
- NSAIDs (except if aspirin at cardiac dose e.g. 75mg od)
- Aminoglycosides
- ACE inhibitors
- Angiotensin II receptor antagonists
- Diuretics
Metformin, Lithium + Digoxin : NOT NEPHROTOXIC but stopped in AKI
Acute Tubular Necrosis
often due to: Ischaemia or Nephrotoxins
damage and death (necrosis) of the epithelial cells of the renal tubules. It is the most common intrinsic cause of acute kidney injury.
- Muddy brown casts on urinalysis confirm acute tubular necrosis
- Renal tubular epithelial cells may also be seen
- The epithelial cells can regenerate, making acute tubular necrosis reversible. Recovery usually takes 1-3 weeks.
Feautures and causes of CKD
Definition: Chronic reduction in kidney function sustained over three months. It tends to be permanent and progressive.
Feautures: oft asymptomatic, Fatigue, Pallor (due to anaemia), Foamy urine (proteinuria), Nausea, Loss of appetite, Pruritus (itching) , Oedema, Hypertension, Peripheral neuropathy, Polyuria
Causes: Diabetes, Hypertension, Medications (e.g., NSAIDs or lithium), Glomerulonephritis, Polycystic kidney disease
Classification of CKD
Factors which may affect the result
- pregnancy
- muscle mass (e.g. amputees, body-builders)
- eating red meat 12 hours prior to the sample being taken
- Estimated glomerular filtration rate (eGFR) is sustained below 60 mL/min/1.73 m2
- Urine albumin:creatinine ratio (ACR) is sustained above 3 mg/mmol
Staging
- 1 > 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests are normal, there is no CKD)
- 2 60-90 ml/min with some sign of kidney damage (if kidney tests are normal, there is no CKD)
- 3a 45-59 ml/min, a moderate reduction in kidney function
- 3b 30-44 ml/min, a moderate reduction in kidney function
- 4 15-29 ml/min, a severe reduction in kidney function
- 5 Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed
A diagnosis can be made when there are consistent results over 3 months
Most common eGFR used:
Modification of Diet in Renal Disease (MDRD) equation, which uses the following variables:
- serum creatinine
- age
- gender
- ethnicity
Complications of CKD
- Anaemia : reduced erythropoietin levels -> low RBC. normochromic normocytic anaemia.perform iron studies before commencing treatment
-
Bone Disease: High serum phosphate
Low vitamin D activity
Low serum calcium
These serum abnormalities lead to more parathyroid hormone release: Secondary Hyperparathyroidism
The following bone diseases seen due to this Osteitis fibrosa cysticae, Adynamic, Osteomalacia, Osteosclerosis, Osteoporosis - Hypertension: most require more than two drugs to treat hypertension
- Proteinuria: Proteinuria is an important marker of chronic kidney disease, especially for diabetic nephropathy. NICE recommend using the albumin:creatinine ratio (ACR)
the NICE guidelines state ‘regard a confirmed ACR of 3 mg/mmol or more as clinically important proteinuria’
Management of CKD
What can slow disease progression?
Treating the underlying cause involves:
Optimising diabetic control
Optimising hypertension control
Reducing or avoiding nephrotoxic drugs (where appropriate)
Treating glomerulonephritis (where this is the cause)
ACE inhibitors (or angiotensin II receptor blockers)
key in the management of proteinuria
they should be used first-line in patients with coexistent hypertension and CKD, if the ACR is > 30 mg/mmol
if the ACR > 70 mg/mmol they are indicated regardless of the patient’s blood pressure
SGLT-2 inhibitors (dapagliflozin)
patients who have proteinuric CKD (with or without diabetes) may benefit from treatment with SGLT2 inhibitors
they primarily act by blocking reabsorption of glucose in the proximal tubule → lowers the renal glucose threshold → glycosuria
by blocking the cotransporter, they also reduce sodium reabsorption → natriuresis reduces intravascular volume and blood pressure, but it also increases the delivery of sodium to the macula densa → normalizes tubuloglomerular feedback and thereby reduces intraglomerular pressure
Management of end-stage renal disease involves:
- Special dietary advice
- Dialysis
- Renal transplant
