Renal Flashcards
What 4 factors affect eGFR?
CAGE -
Creatinine
Age
Gender
Ethnicity
Main Drugs that can exacerbate AKI/CKD?
9 MARKS
ACE-I
Metformin - Lactic Acidosis stop GFR<30
Lithium
Gentamicin
NSAIDS
Ciclosporin
Trimethoprim - Falls exaceberation, cause Se CR++
Furosemide - Releases Na+ so can cause fluid loss
CT Contrast (Iodinated)
Indications for Urgent Dialysis?
AEIOU
A- Acidosis (Lactic, Metabolic, Uremic) - Metabolic acidosis <7.2
E- Electrolytes (Excessively high amounts) - Hyperkalemia >7mM
I - Intoxication
O - Overload (Fluid) - Pulmonary Oedema
U - Uraemia - Pericarditis, Encephalopathy
Name causes for sterile pyuria?
[8 Marks]
Partially treated UTI
Urethritis (e.g. Chlamydia)
Renal stones
Appendicitis
Renal TB
Bladder/Renal Ca
APKD
Analgesic nephropathy
Papillary necrosis
SLE?
Renal Complications + Management
Lupus nephritis can cause end-stage kidney disease.
SLE patients require regular urinalysis to rule out proteinuria.
Stage 3 (focal glomerulonephritis) + 4 (diffuse glomerulonephritis) are started on glucocorticoids + Cyclophosphamide/Mycophenolate
Stage 4 most common and severe form.
Most of bicarbonates are reabsorbed?
Proximal tubules
What’s the best way to differentiate AKI vs. CKD?
Renal US, Bloods
CKD - Smaller bilateral kidneys *
Hypocalcaemia (CKD>AKI)
- Exceptions - HIV, APKD, Amyloidosis, Diabetic Nephropathy
Normal Anion Gap Range?
8-14 mmol/L
Calc: (Na+ K) - (HCO3- + CL-)
Extent of anion gap is used to categorise causes for metabolic acidosis.
Young Female
Fever, Weight loss and Painful, Red eyes.
WHAT COULD IT BE?
TINU (Tubulointerstitial nephritis with uveitis)
Urinalysis is positive for leukocytes and protein.
Acute Interstitial Nephritis
Causes
Presentation
Investigations
Drugs - Abx (Penicillin, aminoglycosides), NSAIDS, Rifampicin, allopurinol, furosemide, PPIs, Diuretics
Systemic disease - SLE, sarcoidosis, and Sjögren’s syndrome
Infection
Fever, rash, arthralgia, eosinophilia, hypertension
mild renal impairment. Typically present with delayed (2-40 days) picture
Investigations - Urinalysis (sterile pyuria, white cell casts)
Histology: marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules
AIN - causes an ‘allergic’ type picture consisting usually of raised urinary WCC, IgE, and eosinophils, alongside impaired renal function
What are the complications of an AV fistula?
Infection
Thrombosis - Absence of a bruit
Aneurysm
Stenosis - Acute limb pain
Vascular access steal syndrome - AV fistula causes ischaemia leading to symptoms
- Pallor
- Diminished pulses (Distal to fistula) , Reduced wrist-brachial BP
- Pain distal to fistula
- Necrosis
What Diagnostic criteria classifies an AKI?
Rise in creatinine of >= 26µmol/L in 48 hours
> = 50% rise in creatinine over 7 days (X1.5 Baseline)
Fall in urine output to <0.5ml/kg/hour for more than 6 hours / 8 hours in children
> = 25% fall in eGFR in children / young adults in 7 days.
Stages of AKI (acute renal failure)
KDIGO Criteria
(Kidney Disease: Improving Global Outcomes)
Stage 1 - Standard AKI
Increase in creatinine to 1.5-1.9 times baseline /
Increase in creatinine by ≥26.5 µmol/L /
Reduction in urine output to <0.5 mL/kg/hour for ≥ 6 hours
Stage 2 - Moderate AKI
Increase in creatinine to 2.0 to 2.9 times baseline/
Reduction in urine output to <0.5 mL/kg/hour for ≥12 hours
Stage 3 - Severe AKI
Increase in creatinine to ≥ 3.0 times baseline/
Increase in creatinine to ≥354 µmol/L/
Reduction in urine output to <0.3 mL/kg/hour for ≥24 hours/
The initiation of kidney replacement therapy (Dialysis/Renal Transplantation)
Patients <18 years, decrease in eGFR to <35
What situations should referral to nephrology occur for an AKI?
Renal transplant
Stage 3 AKI
CKD stage 4 or 5
ITU patient with unknown cause of AKI
Inadequate response to treatment
Vasculitis/ glomerulonephritis/ tubulointerstitial nephritis/ myeloma
Complications of AKI / Uraemia
Fluid Overload (Pulmonary oedema)
suspected AKI secondary to urinary obstruction
Complications of an AKI?
Electrolyte Disturbances - Hyperkalemia - Risk of arrhythmias, HyperPHOS , HypoCA,
Metabolic acidosis
Anaemia
Bleeding - Platelet dysfunction
Infection - WBC dysfunction
Uremic encephalopathy
Pericarditis
Fluid overload
Stress GI Ulcers
Complications of Uraemia?
Gout
CKD
Uric Acid Stones
What are the common risk factors for developing an AKI?
[10 Marks]
Age >65 years
CKD - eGFR < 60
Diabetes
Heart failure
Liver disease
Emergency surgery - risk of sepsis/hypovolaemia
Intraperitoneal surgery
Nephrotoxic drugs
Use of iodinated contrast agents within the past week
History of acute kidney injury
Extra - Rise in molecules that the kidney normal excretes/maintains a careful balance of - e.g. potassium, urea and creatinine
What is the most effective form of Kidney/Renal replacement therapy?
Transplant
Peritoneal dialysis
What Investigations should all patients presenting with an AKI have?
Urinalysis
Renal US - Within 24Hrs
Bloods - U+E, FBC, etc…
Management for AKI?
Largely supportive
Careful fluid balance - Maintain adequate perfusion and not to reduce fluid overload
Stop all nephrotoxic drugs
Close monitoring of electrolytes
If fluid overload (Loop diuretics)
How much protein does +1 Urine dipstick equal to?
Proteinuria
+1 = 30mg/dL
+3 = 300mg/dL
Explain how peritoneal dialysis works?
Administering dialysis fluid into the peritoneal cavity.
Waste solutes diffuse into the dialysate across the peritoneum (Acts as a semi-permeable membrane).
Ultrafiltration (draws water in from the peritoneal cavity) occurs by the addition of osmotic agents to the dialysate (typically 1.5% glucose solution).
Complications of peritoneal dialysis?
Peritoneal dialysis peritonitis (Staph. Epidermis)
Abdo pain, fever, cloudy dialysis bag- (sent for culture)
Intraperitoneal + systemic abx needed.
Catheter malfunction
Obesity (absorption of glucose from dialysis fluid)
Hernias
Explain how Haemodialysis works?
Counter-current flow is created.
Blood and dialysis fluid flow on opposite sides of the semi-permeable membrane. Solute transfer occurs by diffusion.
Complications of Haemodialysis?
Cardiovascular disease
Fistula complications
Hypotension
Amyloidosis (secondary to build up of B2 microglobulin)
Dialysis disequilibrium syndrome (acute cerebral oedema due to rapid extraction of osmotically active substances)
CYSTITIS
Definition?
Clinical features?
Investigations?
Management?
D- INFLAMMATION OF THE BLADDER (UTI affecting the bladder)
Transuretharal ascent of colonic commensals (e.coli)
CF - Urinary frequency, Dysuria, Urgency
Foul-smelling urine, Suprapubic pain / suprapubic tenderness
Ix - Urine Dip +Leuckocytes +Nitrites
++Mid-Stream urine sample only (Children, Men, Pregnancy)
Rx- Nitrofurantoin / Trimethoprim
Advise - Post-coital voiding, regular fluid intake
PYELONEPHRITIS?
Definition?
Clinical features?
Investigations?
Management?
D - Inflammation of the kidneys (UTI affecting kidneys/renal pelvis)
Transuretharal ascent of colonic commensals (e.coli)
CF- Fever/rigors, Malaise, Loin/flank pain, Vomiting, Flank tenderness, renal angle tenderness.
Ix - Urine Dipstick +leukocytes +nitrites
Bloods - FBC(++WCC), U+E (renal impairment?), Renal US, Midstream Urine sample (microscopy, culture and sensitivity)
Rx- Hospital IV Abx (broad-spectrum cephalosporin/a quinolone/gentamicin)
How to distinguish Pyleonephritis from Cystitis?
Cystitis- No pyrexia or have flank tenderness.
Abnormal vitals more w/ pyelonephritis.
Common causes of proteinuria?
[8 Marks]
Diabetes Mellitus
Minimal change disease
Membranous glomerulonephritis
Systemic Lupus Erythematosus
Pre-eclampsia
Amyloidosis
Urinary Tract Infection
Acute Tubular Necrosis
Mnemonic for nephrotoxic drugs?
DAAMN G
D - Diuretics
A - ACEI/ARB
A- Aminoglycosides
M - Metformin
N- NSAIDS
G - Gentamycin
Complications of Immunosuprresant Drugs in transplant patients?
A - Steroids
B - Mycophenolate
C - Tactolimus
D- Ciclosporin
A- Cushing syndrome, Avascular necrosis, Addisons
B- GI Upset, Myelosuppresion
C- Cardiomyopathy, Peripheral neuropathy, Diabtes
D- Gingival hypertrophy, Nephrotoxicity, Hypertrichosis (Excessive hair growth)
Define Renal Tubular Acidosis (RTA)?
Impaired acid excretion of the kidneys which leads to HYPERCHLORAEMIC METABOLIC ACIDOSIS
RAAS activation + Potassium wasting (HypoKALEMIA)
What are the types of RTA?
Type 1 - Inability to excrete hydrogen Ions
PH>5.5 - Failure to acidify urine despite the acid load.
Type 2 - Defect in HCO3 Reabsorption in the PCT. Can only acidify urine when HCO3 is LOW (systemic acidosis) Assoc. W/ Fanconi syndrome
Urine will acidify with an acid load (pH <5.5)
Type 1 RTA?
CAUSES
CLINICAL FEATURES
Hereditary: Marfan’s, Ehler’s Danlos
Autoimmune: Sjogren’s, SLE, thyroiditis
Drugs
Rickets/osteomalacia (bone buffering)
Renal stones
UTI
Nephrocalcinosis can lead to end stage renal failure
Type 2 RTA?
CAUSES
CLINICAL FEATURES
Idiopathic
Inherited: inborn errors, Wilson’s
Acquired: tubule damage (drugs, myeloma)
Polyuria (osmotic diuresis)
Hypophosphataemic rickets (Vit D resistant)
Acidosis
Low potassium
FANCONI SYNDROME
EXPLAIN?
Disturbance of PCT function leads to generalised impaired reabsorption of amino acids, K+, HCO3, phosphate and glucose
Renal Tract Stones (Urolithiasis)
What are the 6 Main renal stones?
Calcium (Most Common 80%) - Calcium oxalate (Increase urinary ca+ /phospate (High protein diet). Opaque stones
Uric Acid (Urate) - Gout increased risk factor, Radiolucent
Struvite - Staghorn Calculi (Renal pelvis + extend into 2+ renal calyces), Proteus mirabilis infection, Recurrent Upper UTI Increased risk factors
Cysteine - Homocysteinuria (Auto Recessive) risk factor, cystine leak into urine (semi-opaque)
Indinavir (HIV Med) - Radio-lucent (Non-visible on any scans), Rare form
Xanthine - Xanthine oxidase deficiency (can’t be oxidised to uric acid)
Investigations for renal stones?
Non-contrast CTKUB
Bloods - Renal func (U+E)
Management of renal stones?
<5mm Asymptomatic? - Watchful waiting, Spontaneous passing
Percutaneous Nephrolithotomy- >2cm Large stones, Staghorn calculi, cysteine stones,
Catheter, Needle, Forceps extraction (used to fragment stones) through cystoscope
Ureteroscopy - Distal/middle uteric stones, pregnant women, flexible or rigid
Shock wave lithotripsy - High energy shock waves with help of fluoroscopy, energy fragments stone
Open surgery - staghorn calculi/complex renal tract anatomy
Prevention - Allopurinol/Potassium citrate for uric acid stones
Thiazides - Hypercalcuria
Supportive - Fluids, Avoid NSAIDS
Clinical features of renal stones?
Severe, Intermittent loin pain with radiation to the groin
Restless patient
Haematuria - Macroscopic/Microscopic
N+V
Secondary infection of stone -> Sepsis (Surgical emergency = Urgent decompression)
What is the TRIAD of AKI symptoms?
Oliguria
Uraemia
Electrolyte imbalance
Acute Tubular Necrosis (ATN)
Define?
Causes?
Management?
Intrisic cause of AKI. Damage to tubular epithelial cells within renal tuules of kidney due to ischaemia or direct toxicity
Ischaemia - Hypotension, Shock (Cardiogenic, Septic, Haemorrhagic), Vascular injury - Trauma/Surgery
Nephrotoxic Drugs -DAAMN G
- Statins, Cisplatin, Iodinated contrast
Correction of underlying cause
-Fluid resus, Drug review (Removal of nephrotoxins)
ADPKD - Genetic cause of chronic renal failure in adults
Causative Chromosome defects?
Features - Renal, Extra-renal ?
Causes of death in ADPKD ?
ADPKD1 - C16 (Polycystin-1) - More severe 85%
ADPKD2 - C4 (Polycystin- 2)
Defect in epithelial cell differentiation and/or extracellular matrix function.
Cystic dilation of renal tubular epithelium, Expanding cystis cause bilateral kidney enlargement + destruction of renal parenchyma.
Fluid-filled Cysts in renal cortex + medulla (Clear, turbid/haemorrhagic)
Renal - Haematuria, Flank pain, renal dysfunction, HTN, Microalbuminuria, bilateral kidney enlargement.
Extra-Renal - Cysts( liver, Pancreatic, spleen*), Mitral valve prolapse, Colonic diverticular, Intracranial berry aneurys - Junction of ACommA, ACA, hernias
Common Causes of death - SAH (Berry Aneurysm), Intracerebral Haemorrhage, Infection, Heart Disease
*Very rare to get splenomegaly
Causes of urinary retention?
Investigations for urinary retention?
Causes - Neurological, Obstructive. Infectious, Post-operative, Drugs (Anticholinergics, A-Agonists)
Anticholinergic classes of medications block sympathetic activity on the detrusor muscle and their inhibitory effects on the bladder sphincters.
Drugs with alpha agonist properties inhibit bladder contraction and cause sphincter contraction.
Ix - Bladder scan, Digital Rectal Exam, Urinalysis, Post void residual
What clinical picture dose Anti-Glomerular basement membrane disease (Goodpasture’s disease) show?
Haemoptysis +AKI + proteinuria/haematuria
Exacerbated by respiratory tract infection.
Goodpasture’s Disease (Anti-GBM disease)
Features
Investigations
Management
D- Rare type of small-vessel vasculitis associated with both pulmonary haemorrhage and rapidly progressive glomerulonephritis. Anti-GBM antibodies against Type 4 collagen. Antibodies are directed against antigens that are found on the glomerular basement membrane in the kidneys and in the lung alveoli.
Clinical Presentations -
Pulmonary haemorrhage,
Rapidly progressive glomerulonephritis (rapid onset AKI -> nephritis -> Proteinuria +haematuria)
Investigations
Renal Biopsy - Linear IgG deposits along basement membrane
Raised Transfer Factor (2* Pulmonary haemorrhages)
Rx - Plasma exchange (plasmapheresis), High dose steroids (prednisolone), cyclophosphamide (chemotherapy)
What risk factors increase the likelihood of pulmonary haemorrhages in patients with Goodpasture’s ?
Smoking
LRTI
Pulmonary Oedema
Young male
Hydrocarbons inhalation
HLA-DR2
Bimodal distribution (20s + 60+)
Alport Syndrome
Main clinical presentation?
Microscopic haematuria, bilateral sensorineural deafness, and lenticonus.
Diabetic Nephropathy
Main clinical presentations?
Microalbuminuria and glucosuria.
Post-streptococcal Glomerulonephritis
Main clinical presentations?
Haematuria and Haemoptysis, as well as proteinuria.
Has had an Group A beta-haemolytic Strep infection recently (1-2 weeks)
Minimal Change Disease?
Causes
Pathophysiology
Investigations
Management
Prognosis
C - Idiopathic (Most Commmon), Hodgkin’s lymphoma, thymoma, infectious mononucleosis, Nephrotoxic drugs.
Pathophys- T-cell and cytokine-mediated damage to the glomerular basement membrane (Anion loss).
Total reduction of electrostatic charge = increased glomerular permeability to serum albumin
Ix - Normotension
Renal Biopsy - NORMAL light microscopy
ABNORMAL electron microscopy (podocyte fusion and effacement of foot processes)
Rx - Steroids (80% responsive)
Chemotherapy for steroid-resistant cases (Cyclophosphamide)
Prognosis - 1/3rds
1. 1 episode
2. Infrequent relapses
3. Frequent relapses
Contrast-induced AKI
What fluid treatment is appropriate?
Criteria for Contrast-media nephrotoxicity?
infusion of IV 0.9% sodium chloride at a rate of 1 mL/kg/hour for 12
Pre + Post procedure
25% increase in CR within 3 Days of contrast media administration.
Risk factors for contrast-induced AKI?
Hx of renal impairment
Age > 70
Dehydration
Heart failure
Nephrotoxic drugs
When should metformin be STOPPED in renal impairment?
eGFR<30
When should a GP refer someone with CKD to nephrology?
[9 Marks]
eGFR falls <30 or progressively by > 15 in a year
A sustained decrease in eGFR of 25% or more, and a change in GFR category
Urinary albumin: creatinine ratio (ACR) of 70 mg/mmol or more
A urinary ACR of >30 mg/mmol + persistent haematuria, after exclusion of a UTI.
Hypertension that remains uncontrolled despite use of at least 4+ antihypertensive drugs at therapeutic doses.
A suspected or confirmed rare or genetic cause of CKD (polycystic kidney disease)
Suspected renal artery stenosis.
Suspected complication of CKD.
FSGS (Focal Segmental Glomerulosclerosis)
Causes
Investigations
Management
Focal Segmental glomerulosclerosis is a type of glomerular disease and describes scarring (sclerosis) in your kidney.
Causes - Idiopathic, 2* to other renal pathology e.g. IgA nephropathy, reflux nephropathy, HIV, heroin, Alport’s syndrome, sickle-cell
Ix - Renal biopsy
Focal and segmental sclerosis and hyalinosis on light microscopy
Effacement of foot processes on electron microscopy
[Loss of foot processes on EM]
Rx- Steroids +- Immunosuppressants
Name the Types of Glomerulonephritis?
[8 Marks]
Focal segmental glomerulonephritis
IgA Nephropathy
Membranous Glomerulonephritis
Minimal change disease
Rapidly progressing glomerulonephritis
Lupus nephritis
Post-infectious glomerulonephritis
Anti- Glomerular basement membrane disease (Anti-GBM)
Causes of Glomerulonephritis?
[6 Marks]
Infection- Group A Strep, Hep B/C, Resp infections, GI infections, HIV, Endocarditis
Systemic Inflammatory conditons - Lupus, RA, Anti-GBM, GPA
Nephrotoxic drugs
Maliganancy
Hereditary disorders - Alport’s syndrome
Amyloidosis
Management of glomerulonephritis?
Abx if infection
ACEi to decrease proteinuria*
Corticosteroids
Furosemide if HTN and fluid overload
Immunosuppressant drugs
Plasmapheresis
*ACEi or ARBs are protective for most forms of CKD, particularly those with proteinuria
Mneumonic for conditions that cause a nephritic picture?
SHARP AIM
SLE
HSP (Henoch-Schönlein purpura)
Anti-GBM
Rapidly progressive glomerulonephritis (GN)
Post-streptococcal GN
Alport’s syndrome
IgA Nephropathy (Berger’s disease)
Membranoproliferative GN
Main difference between post-streptococcal glomerulonephritis & IgA nephropathy?
Post-streptococcal glomerulonephritis typically presents 3-4 weeks after a sore throat/skin infection whereas IgA nephropathy typically presents 3-4 days after a mild URTI.
What differences help to decide between NEPHROTIC VS. NEPHRITIC SYNDROME?
Nephritic syndrome - More likely to present with haematuria and non-nephrotic range proteinuria (1+/2+ on the urine dipstick). Hypertension is also more common.
