Renal Flashcards
Defintion & Stages of CKD
Def: markers of kidney damage and/or reduced kidney function over 3mths or more
Stages: G1: eGFR >90 G2: eGFR 60-89 G3: eGFR 45-59 (A) 30-44 (B) G4: eGFR 15-29 G5: eGFR <15
A1: ACR <3 mg/mmol
A2: ACR 3-30
A3: ACR >30
Causes/Risk Factors for CKD
Hypertension Diabetes Older Age (RF) Obstructive nephropathy Ischaemic nephropathy (due to vascular disease) Glomerulopathies Inherited kidney disease e.g. PKD Tubulointerstitial disease Medications e.g. Lithium Smoking (RF)
Clinical presentation of CKD
Generally asymptomatic
Non-specific sx tend to start when eGFR <45
Symptoms: Anoxeria, nausea, weakness, fatigue, muscle cramps, pruritus, dyspnoea
Signs: fluid overload, pallor (anaemia), hypertension
Investigations for CKD
U&Es - eGFR, hyperK
Urinalysis - dipstick for haematuria (consider 2WW), ACR
Renal USS +/- biopsy - if considering PKD or obstructive picture
Management of CKD
- Renoprotection - BP control (ACEI & aim <140/90), statin therapy, antiplatelet therapy & lifestyle (stop smoking)
- Treat complications - anaemia (EPO stimulating agents or Fe infusions), hyperK (monitor U&Es, CKD & ACEI both can cause), bone & mineral disorders (VitD supplements, low phosphate diet, bisphosphonates for osteoporosis)
- RRT - dialysis, peritoneal dialysis or renal transplant
Definition & Criteria for AKI
Acute decline in renal function occurring over hours/days
Rise in Cr >25 umol/L in 48hrs or >50% in 7days
Urine output <0.5ml/kg/hr for >6hrs
Causes of AKI
Pre-renal; hypovolaemia, reduced cardiac output, systemic vasodilation
Renal; vascular (thromboembolic, dissection, stenosis), glomerular, tubulointerstitial (ATN)
Post-renal; obstruction (stones, malignancy, BPH)
Investigations for AKI
History (meds) & examination (fluid status)
Bloods - guided by cause (FBC, U&Es, ABG)
Urinalysis for protein, blood, leucocytes, nitrites and glucose.
Leucocytes and nitrites suggest infection
Protein and blood suggest acute nephritis (but can be positive in infection)
Glucose suggests diabetes
Ultrasound of the urinary tract is used to look for obstruction. It is not necessary if an alternative cause is found for the AKI.
Management of AKI
Prevention - hydration& med reviews
Treat/reverse cause: hydrate (pre renal), stop nephrotoxic meds (renal), reverse obstruction (post renal)
Consider specialist input if AKI stage 3 or post renal AKI
RENAL DRS 25 Mnemonic
Record baseline Cr & regular U&Es Exclude obstruction Nephrotoxic drugs stopped Assess fluids status Losses +/- cauterisation Dipstick - blood/protein Review medications Screen - acute renal screen 25 - rise in Cr = AKI
Urinary Calculi - composition, clinical features
Types: calcium phosphate/oxalate (80%), magnesium ammonium phosphate (10-20%)
• Can be asymptomatic • Loin to groin flank pain a/w nausea & vomiting ○ May also radiate to testicles, abdominal area • Sharp, sudden, severe pain - may be intermittent • Haematuria ○ can be microscopic or frank • Dysuria Urinary frequency/urgency/retention
Urinary Calculi - investigations & management
Bedside
• Observations - HR, BP, temp (check if septic)
• Examination
• Urinalysis - dipstick, microscopy, C&S (r/o UTI & check for haematuria)
Bloods
• FBC inc WCC
• U&Es (check renal function, hydration status, AKI)
• Calcium, urea & phosphate levels
Imaging
• X-ray KUB - 90% of stones are radio-opaque so should show on X-ray
• USS - can be used to show any dilatation or if radiation is CI
• Conservative/medical - observation, analgesia, fluids (IV or oral), alpha blockers to help with ureteric relaxation ○ Suitable if stones are <5mm, should pass • Removal of calculi - ureteroscopy ○ Indicated if obstructed stone or continued pain or pyrexia • Lithotripsy - non invasive, break up stone into smaller fragments to allow it to pass if stone <2cm & no obstruction
Definition of Nephrotic Syndrome
Syndrome with a triad of heavy proteinuria >3.5g/day, hypoalbuminemia and oedema
Structural damage to basement membranes leads to loss of protein & albumin
Clinical Features of Nephrotic Syndrome
Signs of fluid overload Fatigue SOB Peripheral oedema Pulmonary oedema Swelling of face, abdomen & genitals Foamy urine - due to protein Poor appetite Haematuria
Investigations - Nephrotic Syndrome
Diagnosis based on presence of classical triad of symptoms
• Urinalysis
• Bloods - FBC, U&Es, LFTs (albumin), glucose, lipids, ESR/CRP
• Renal biopsy - usually needed to determine diagnosis
Management - Nephrotic Syndrome
Treat oedema • Fluid & Na restriction • Diuretics - furosemide Treat cause • For example - minimal change --> high dose steroids +/-immunosuppression
Monitor
• Blood pressure
• U&Es
• Fluid chart & weight
Manage complications
Complications - Nephrotic Syndrome
• Thromboembolic disease ○ Anticoagulation • Hyperlipidaemia ○ Statin therapy • Recurrent infections • AKI/renal damage
Definition & Aetiology - Nephritic Syndrome
the presence of haematuria, variable proteinuria, renal impairment, and hypertension.
Post Streptococcal Glomerulonephritis (esp. Group A beta-Haemolytic Streptococcus)
IgA Nephropathy - Berger’s Disease - the commonest Glomerulonephritis
Vasculitis/SLE
aetiology of polycystic kidney disease & clinical presentation
Inherited AD condition - mutations in PKD1 (80%) & PKD2 (20%)
May be asymptomatic, often presents in 30/40s can be incidental
Flank/abdo/back pain - large cysts or ruptures
Haematuria - ruptures
Polyuria/polydipsia/nocturia
Large palpable kidneys
Hepatomegaly
Hypertension
Investigations & Management of Polycystic kidney disease
Bloods (U&Es, Cr, eGFR) & urinalysis (dipstick, C&S, microscopy & ACR)
Diagnosis on imaging - CT/USS will show multiple cysts & enlarged kidneys, >2 cysts on patients <30
BP control (ACEi) - slows decline of renal function RRT/dialysis - by 60s half of p
Risk factors for Pyelonephritis
Obstructed urinary tract, including BPH
Spinal cord injury, resulting in a neuropathic bladder
Female gender (due to a short urethra)
Indwelling catheter or ureteric stents / nephrostomy tubes in-situ
Structural renal abnormalities, such as vesico-ureteric reflux (VUR)
Diabetes mellitus, corticosteroid use, HIV infection (untreated)
Renal calculi Sexual intercourse Oestrogen depletion (menopause)
Clinical Features - Pyelonephritis
fever, unilateral loin pain (or rarely bilateral), and nausea & vomiting, typically developing over the course of 24-48 hours.
(frequency, urgency, dysuria), as well as visible (or non-visible) haematuria.
Differential Dx - Pyelonephritis
potential ruptured AAA.
Other differentials include renal calculi, acute cholecystitis, ectopic pregnancy or pelvic inflammatory disease, lower lobe pneumonia, or diverticulitis
Investigations - Pyelonephritis
Bedside
• Observations - temp (suspicion of sepsis)
• Urinalysis - dipstick, C&S, microscopy
• Pregnancy test - if any lady of child bearing age
Bloods
• FBC - WCC, Hb
• CRP/ESR - inflammation
• U&Es - dehydration, renal function, electrolytes
• LFTs
• Amylase - r/o pancreatitis
Imaging
• All cases of pyelonephritis should have a renal US scan performed for evidence of obstruction (as an infected obstructed system is a urological emergency)
• If obstruction is suspected, non-contrast CT imaging of the renal tract should be performed (CT KUB).
Management - Pyelonephritis
Start empirical antibiotics based on local protocols and IV fluids as appropriate
Tailor once sensitivities are available
Analgesia and anti-emetics
Whilst many uncomplicated cases can often be treated in the community, consider admission in those cases who are clinically unstable, significant dehydration, or with co-morbidities such as diabetes mellitus, renal transplant graft, immunocompromised
IgA nephropathy - pathophysiology, S&S, investigations & management
Most common primary glomerulonephritis - occurs when IgA immune complexes deposit in kidney in the renal mesangium, causing damage
Macroscopic haematuria (a/w infections e.g. URTI, gastroenteritis), asymptomatic micro haematuria & proteinuria, hypertension, loin pain, low grade fever
observations(BP), urine dipstick & microscopy, bloods (baselines n U&Es), USS KUB
diagnosed via kidney biopsy - H&E stain, immunofluorescence, electro micro
lifestyle measures (w/l, stop smoking, diet), ACEI/ARB to control BP, steroids no longer used routinely as shown to be no benefit - reserved for special cases & in those where renal function is deteriorating significantly
