Renal Flashcards
Hypertension: Classifications
Classification: Primary, Secondary, Malignant
Causes of secondary HTN
- Drugs: NSAIDs, corticosteroids, COCP, alcohol, Tacrolimus, Ciclosporin
- Renal disease: CKD, Renovascular disease, AKI
- Endocrine: Hyperthyroidism, hypothyroidism, pheochromocytoma, cushing’s syndrome, Conn’s syndrome
- Systemic disease: SLE, systemic sclerosis, vasculitis
- Other: Pre-eclampsia, coarctation, OSA
Signs of malignant hypertension: MAHA, impaired vision, headaches. Due to high pressure in small vessels
Hypertension: Management protocol
- Clinical BP measuring:
<140/09 –> recheck in 5 years
140/90 - 179/119 –> Assess end organ damage, calculate CV risk, send of ABPM
>180 / 120 –> consider starting medication immediately - At ABPM
<135/85 –> recheck in 5 years
Stage 1 HTN of 135/85 - 149 /95 –> Offer lifestyle advice. Consider starting drug therapy if >80 with clinic BP of >150/90, <80 with end organ damage/>10% CV risk / DM / Renal disease / CVD or <60 with CV risk <10%.
Stage 2 HTN of >150/95 –> Lifestyle advice and drug treatment - Annual review
* All diabetics on ACEi/ARB regardless of BP
Antihypertensives
What drugs?
If <55 years old, start with ACEi
If >55years old or afro-carribbean, start with calcium channel blocker.
Target:
<150/90 for all >80s
<140/90 for all <80s or those with CKD
<130/80 for all those with proteinurea and diabetics
Common side effects: ACEi - Dry cough, dizziness ARB - Dizziness CCB - Swollen ankles, flushing, headache, dizziness Diuretics- Urinary frequency, dizziness
Sick day rules: Stop these meds to prevent AKI “DAMN”
- Diuretics
- ACEi / ARB
- Metformin
- NSAIDs
HTN risk stratification
Scoring:
- Qrisk
- Ketih-Wagener Barker for HTN retinopathy (Grades 1-2 have no ocular symptoms. Grade 3 has retinal haemorrhages, exudates, cotton wool spots, retinal artery sclerosis. Grade 4 has all of Grade 3 with papilloedema)
- ECG for left ventricular hypertrophy (Prominent S wave in V1/2, tall R waves in V5/6)
Obstruction
Anatomical result: Hydronephorosis, hydroureter
Presentation:
If lesion above the bladder –> Renal colic (intermittent, sudden, aching in the loin), neurological causes
Infection –> Malaise, haematuria, dysuria, fever
If complete obstruction–> Anuria
Partial obstruciton –> Oligouria with patadoxical polyuria
Investigations
1st line Renal function (Deranged in bilateral obstruction), FBC, USS KUB (check for dilatation of bladder and collecting systems), Urine culture (to exclude infection)
2nd line: If ureters involved CT/MRI, pyelography
Management
Immediate: Nephromstomy
Definitive: Remove obstruction, treat complication and IV fluids to balance polyuria
CKD
Definition: eGFR<60 on 2 occasion for than 90 days apart +/- kidney damage markers
Cause:
- DM *
- Interstitial nephritis *
- Glomerulanephritis *
- HTN
- Inherited: Alphort, PKD
- Renovascular disease
Risk factors:
- DM
- HTN
- CVD
- Nephrotoxic drugs
- Obstructive uropathy
- Hx of AKI
Ix:
1st line
- eGFR (to stage)
- ACR (to risk stratify, should be <3mg/mmol)
- CV assessment (glucose, HbA1c, lipids)
- LFTs
- Electrolytes
- Urinalysis
2nd line
- Renal USS if indicated (to distinguish between AKI and CKD)
- Biopsy if indicated (PCR>100mg, rapid eGFR decline, suspected systemic disorder)
- CT or MR angiography if renal artery stenosis suspected
-?Myeloma or vasculitis screen
Staging by KDOQI:
- Stages 1-5 (health - bad)
- Stage 3 a/b most common (eGFR or 30-59)
- Stage 4 (eGFR 15-29): If progressive plan for ESRF
- Stage 5 (eGFR <14): Start dialysis once eGFR <10.
Referral indictions: • eGFR<30 mL/min/1.73 m2. • Accelerated progression of CKD. • Urinary ACR>70 mg/mmol, unless known to be associated with diabetes mellitus. • Urinary ACR >30 mg/mmol with persistent haematuria,after exclusion of a UTI. • Uncontrolled hypertension. • A rare or genetic causeof CKD. • Suspected renal artery stenosis. • A suspected complicationof CKD.
Management in secondary care
- Prevent progression (BP control, ACEi for proteinuria, HCO3 for acidosis)
- Manage complication (Anti-HTN, diuretics for fluid retention, recombinant EPO, Alfacaldidol, PO4 binders, Diet changes of low K, Na, PO4, fluid restriction)
- Prepare for ESRF (6-12 months before patient predicted to reach eGFR of <10. Options of dialysis or transplantation, so either arrange for fistula creation or transplant assessment)
Monitoring:
- BP to be <140/90
- eGFR and ACR for progression
- FBC (Hb for renal anaemia. Electrolytes and PTH for renal metabolic and bone disorder)
Complications:
- AKI
- HTN
- Renal anaemia (Due to 1. iron deficiency shown by TSAT <20% which indicated IV iron 2. Low EPO secretion by adrenals)
- CKD mineral bone disorder (High PO4 and low Ca lead to secondary PTH. Calcium oxalate or Calcium acetate used to treat hyperphosphataemia)
- ESRD
Tubulointerstitial nephritis
CLASSIFICATIONS: Initial (AIN) or chronic (CIN)
PATHOPHYSIOLOGY Causes of AIN: - Allergic (Drugs e.g. NSAID, PPI, Antibiotic, mesalazine. Renal transplant rejection) - Infective (Viral infections - Noxious (Herbal, foods, myeloma casts) - (Autoimmune)
Causes of CIN:
- Allergic and immune (Sarcoid and autoimmune esp Sjogren’s)
- Infective (chronic pyelonephritis)
- Toxic (Ig Light cahins, heavy metals, tacrolimus, cyclosporin, Lithium, Tenofovir)
PRESENTATION
Few or no symptoms
AIN –> Fever and poor renal function
INVESTIGATIONS
1st line:
Dipstick: No or minimal haematuria and proteinuria. May be positive for WBC
U+Es: Renal impairment?
Suspect drug induced AIN? Serum FBC eosinophil count “bland unanalysis and eosinophilia”
MANAGEMENT
1st line if drug cause: Withhold drugs and give few weeks steroid.
RENAL ASSOCIATIONS WITH CIN
- Developmental / congenital (Reflux nephropathy and renal dysplasia)
- Inherited (e.g. Wilson’s disease, cystinosis)
- Ischaemia / papillary necrosis (sickle cell nephropathy or analgesic nephropathy)
TINU
What? Tubulointerstitial nephritis with uveitis)
Who? Young females
Symptoms? Fever, weight loss, painful red eyes
Ix: Urinalysis positive for leukocytes and protein
Renal Artery Stenosis
*Most common cause of renal vascular disease
Cause:
- Atherosclerosis
- Takayasu’s arteritis
Pathology:
RAAS upregulation –> Treatment resistant HTN and renal function
10% have acute decompensated HF leading to “flash pulmonary oedema”
Presentation:
- HTN
- CKD
- Pre-renal AKI
Investigations:
1st line Renal USS and CT/MRI angiography
Management
1st line - CV risk factor modification (Statin, Aspirin, Anti-HTN using CCB)
2nd line - If flash oedema or rapid /oligo anuric renal failure? Consider revascularisation
Fibromuscular dysplasia
Definition
Non-atherosclerotic, non-inflammatory disease of blood vessels that causes abnormal growth within the artery wall. Most commonly it affects the walls of renal and carotid arteries.
This growth can either be narrowing (stenosis) or enlargement (aneurysm)
Incidence
2nd most common cause of renal vascular disease (10%)
Who?
Females
Features - Hypertension - CKD - AKI (e.g. due to ACEi initiation) "Flash pulmonary oedema"
Thrombotic microangiopathy
i.e. diseases associated with plt dyfunction in small blood vessels and consequent thrombocytopaenia
Examples: TTP and HUS
Pathology: Dysordered plts lead to endothelium damage Precipitators: - Pre-eclampsia / post partum - GvHD - Drugs (quinine , cytotoxic) -Ecoli -Inherited complement abnormalities
Investigations 1st line: - Bloods (Microscopic anaemia, MAHA, LDH raised, raised creatinine, complement levels) Coag screen (normal) -Blood film (RBC fragments) - Stool culture (ecoli?)
TTP
Thrombotic Thrombocytopaenic Purpura (TTP)
Relevance to renal disease: Haematological and CNS manifestation with less severe renal disease (thrombotic microangiopathy)
.
Cause: Deficiency of ADAMTS13 (a metalloprotease enzyme) which cleaves von Willebrand’s factor
Who? Rare, adult females
Pentad of features:
- Fever - Fluctuating neuro signs (microemboli) - MAHA - Thrombocytopaenia - AKI
Management
1st line - Haem emergency get help! Requires plasma exchange (to correct vWF factor def)
2nd line - Consider corticosteroids and rituximab
HUS
What? Type of thrombotic microangiography
Who? Young childrem
Result: Triad of MAHA, AKI and Thombocytopaenia
Cause: Infective (shiga toxin from E.coli, pneumococcal, HIV) or non-infective (SLE, cancer, drugs)
DDx:
- TTP
- DIC
- MAHA
Ix: Stool culture, U+Es, FBC
Mx: Supportive care with fluids, transfusion. No Abx given. plasma exchange reserved only for severe, non-diarrhoeal cases.
HIV nephropathy
Impact of HIV on the Kidneys:
DIRECT: HAART if nephrotoxic, anti-virals crystal formation risks pre-renal AKI and anti-virals risk interstitial disease (e.g. Fanconi syndrome with Tenofovir)
INDIRECT: Susceptibility to infection, HAART-induced metabolic syndrome
Renal manifestations of HIV
Africo-caribbean: Classically “collapsing” FSGS
Non-black races: HIV-ICK
Presentation: HIV associed FSGS - Proteinuria - Metabolic syndrome - Progressive renal failure
Management:
1st line: HAART, ACEi, BP control
2nd line: RRT
What is Fanconi syndrome? How does it present?
Tenofovir induced kidney interstitial disease
Manifesting as: Phosphaturia, glycosuria, normoglycaemia and amino aciduria
SLE nephropathy
Meaning: Systemic Lupus Erythematous
Epideimiology: Young people, more common in blacks and east-asians. 50% of SLE have renal implications, mostly minor
Presentation:
- Fever
- Rash (“butterfly across face)
- Joint pain (*hands)
- Pleuritis
- Nephrotic syndrome)
Ix:
1st line: Antibody screen (anti-dsDNA positive, ANA positive), Biopsy shows proliferative diffuse FSGS, Complement low
Presentation:
- Proteinuria
- Haematuria
- HTN
Management:
Disease control via Immunosuppression (1st line Steroids AND MMF. 2nd line cyclophosphamide
Once ESRF reached - RRT (dialysis or transplanation)
Diabetic nephropathy
Onset:
T1DM within 10-20 years of diagnosis
T2DM present at onset
Defintion: Any form of diabetes with…..
- Microalbuminuria
- Evolving HTN
- Declining renal function
+/- associated diabetic microvascular complications (e.g. retinopathy)
Incidence
1/3 of diabetics
Risk factors for worse prognosis
- Poor glycaemic control
- HTN
- Long duration of diabetes
- FH of HTN or other renal diseases
- Pther microvascular complications e.g. neuropathy or retinopathy
Progression Stage 1+2: Hyperfiltration - Elevated GFR and normoalbuminuria Stage 3: Incipient nephropathy - ACR>3mg/mmol (early) - Positive dipstick for proteins (mid) Stage 4: Overt nephropathy - Nephrotic syndrome -Hypertension Stage 5: ESRF
Investigation: Staging - - ACR - GFR - Clinical presentation Diagnosis: Consider biopsy if indicated (Indications: Progressive albuminuria, HTN. Haematuria, no retinopathy, other systemic symptoms, rapid renal function deterioration, T1DM <10 years) Findings: Glomerulosclerosis, atherosclerosis, nodularity of the mesangium in glomeruli)
Management:
1st line for all diabetics
-Control BMs (HbA1c <7% for T1DM, <7.5% for T2DM)
-Control BP if proteinuria i.e. males ACR >2.5 or >3.5 in females (use ACEi or ARB, check U+Es within 2 weeks. Target <130/80. If PCR >100 then target <125/75.)
- Can use cangliflozin (SLGT2 inhibitor) to control glucose and bp
- CV risk factor management (Smoking, diet, exercise, stress)
2nd line for those with ESRD
- Conservative management
RRT
Screening: Annual 1. Microalbuminuria - T1DM 5 years after diagnosis - T2DM from diagnosis. 2. Renal function for all
Sarcoid and the kidneys
Sarcoidosis is a rare condition that causes small patches of red and swollen tissue, called granulomas, to develop in the organs of the body. It usually affects the lungs and skin.
Epidemiology
F>M
Usually presents in 20-40s
Presentation: (organ dependent but typically)
- tender, red bumps on the skin (e.g. erythema nodosum)
- shortness of breath
- a persistent cough
Renal manifestation:
- Kidney stones
Ix:
- CXR or CT
- Bronchoscopy and biopsy
Mx: Often self limiting. If progressive then Steroids
Myeloma
What? B cell neoplasm that leads to overproduction of monoclonal antibodies
Pathophysiology
- Hypercalcaemia
- Cast nephropathy “myeloma kidney” due to toxicity of light chain in the tubules
- AL amyloidosis
- Deposition diseases
Presentation:
Typically: Few S/S, renal failure can occur after using contrast
Features: CRAB
Management: Chemotherapy
