Renal

Dr T Jenyon

Plan

• Background• Symptoms and Signs• Renal medicine• Renal failure• Rare renal• UTI and calculi• Surgical renal

Background

• Kidney is retroperitoneal• 11-14cm in length• Has a high proportion of cardiac output• Central role in fluid and electrolyte balance

Background

• Other roles:– Erythropoetin– Vitamin D metabolism– Caltabolism of small proteins (insulin)– Drug excretion

Background - Fluid and electrolytes

• ADH (posterior pituitary) controls Osmolality

• Renin-angiotensin-aldosterone controls Extracellular volume (via Na)

Background – Urea and creatinine

• Urea – nitrogenous waste due to breakdown of amino acids

• Raised in• Renal failure• High protein intake• GI bleed (acts as high protein meal)• Dehydration

• Creatinine• Raised in

• Renal failure• Large muscle mass• Acute muscle damage

Notes

• Alcoholics tend to have a very low urea as poor diet and knackered liver

• Sudden increase in Urea but not creatinine think dehydration or GI bleed• Ratio should be around 1:20• Altered ratio (1:5) suggests acute renal failure, GI bleed etc

• Low Hb, high urea, think GI bleed

Renal anatomy

Symptoms and signs

• Frequency/Polyuria• Oliguria• Dysuria/pain• Incontinence• Palpable kidneys• Glycosuria • Haematuria• Proteinuria

Frequency / Polyuria

• Frequency implies increaed frequency voiding – different from polyuria (increased volume)

• Frequency – Think UTI• Polyuria

• Excess intake• Osmotic diuresis (DM)• Defective concentrating ability of kidney

• Diuretics• CRF• Diabetes insipidus

Oliguria• Urine output <0.5ml/kg/hr or less than 400mls per

day

• Causes (basically causes of ARF)– Pre-renal - Decreased perfusion of kidneys

• shock/hypovolaemia– Renal

• ATN/GN– Post renal - Obstruction of urine flow

• Intra-lumen – stone• In the wall – stricture/tumour• Compressing wall – prostate/tumour/AAA

• Remember blocked catheter if catherised

Dysuria/Pain

• Dysuria – pain on urination– Think of UTI/STI– Can get sterile urethritis

• Renal stones classically cause ‘renal colic’– loin to groin pain coming in waves, makes patient

roll around

Incontinence• Involuntary voiding of urine

• If new onset suspect UTI, in men suspect protatism and overflow – check for bladder

• Types:– Functional, i.e. caught short

– Stress, weak pelvic floor, small amounts leak when coughing or laughing • Do pelvic floor exercises, can try Duloxeteine, TFVT or colposuspension is surgical

option

– Urge, uncontrolled emptying of bladder, e.g. brain damage. • Find cause, try timed voiding, oxybutynin/tolterodine can help

Palpable kidneys• Bilateral palpable kidneys

– ADPKD– Bilateral hydronephrosis– Amyloid– Bilateral RCC– Tuberous sclerosis

• Unilateral palpable kidneys– RCC– Hydronephrosis– Bilateral cause with only one palpable

• (In chronic renal failure kidneys tend to be small and shrunken)

Kidney Vs Spleen

• Kidney– Moves late on

inspiration– Possible to get above– Smooth shape– Resonant to percussion

• Spleen– Moves early on

inspiration– Can’t get above– Notched leading edge– Dull to percussion– Enlarges towards RIF

Glycosuira

• Blood glucose of >10mmol will spill over into urine

• Think DM• Can have congenital low renal threshold for

glucose

Haematuria

• Is it Blood?– Rifampicin, beetroot, myoglobinuria

(rhabdomyolysis)• Is it from urological tract

– DD Vagina/rectum• Is it from kidney

– Look for red cell casts• Is it painless

– Think cancer

Haematuria

• Generalised disorder– IBE, coagulopathy, sickle cell, vasculitis

• Specific disorder– Kidneys or Ureter/bladder/Urethra

• Medical– GN – IgA or thin BM disease– Infection - UTI/prostatitis/schistosomiasis

• Surgical– Stone, tumour, trauma

Proteinuria• Urine Dipstix react to albumin but not Bence Jones Protein (myeloma)

• ‘microalbuminuria’ is proteinuria in the range of 30-300mg/L (e.g. DM)

• Quantify proteinuria with 24hr urine of protein/creatinine ratio (PCR) or albumin creatinine ratio (ACR)

• >3.5g/day suggests nephrotic syndrome this may make the urine frothy

• Proteinuria and heamaturia with red cell casts suggests Nephritic syndrome

Proteinuria• Benign

– Orthostatic proteinuria– Exercise/febrile illness

• Excess circulating protein– Myeloma

• Renal damage– DM/GN/nephritic/nephrotic syndrome

• UTI

Renal Medicine

Nephrotic syndromeNephritic syndromeGNTIN

Renal Medicine• Appears complex no definitive relationship

between syndromes/symptoms and pathology/biopsy

• But – Some patterns are present – Results from biopsy can help guide treatment

• E.g. kid presents with nephrotic syndrome:– They are assumed to have minimal change GN. – Treat with Steroids.– If they do not respond to steroids they will have a

biopsy that might reveal a different cause that might need a different treatment

Nephrotic Syndrome

• Massive proteinuria (>3.5g/day)• Hypoalbuminaemia (<30g/L)• Oedema• Hyperlipdaema

• Increased thrombotic tendency (loose antithrombin III and protein S)• Increased susceptibility to infection (loose immunoglobulins)

Nephrotic syndrome

• Commonest cause in kids:– Minimal change glomerulonephritis

• Not much to see on microscopy (minimal change), get fusion of podocytes on electron microscopy

• Benign (only 1% progress to ESRF), treat high dose (60mg) Prednisolone, only biopsy if not responding

• Commonest in adults– Membranous nephropathy

• Thickened BM with spikes on silver staining (IgG)• 1/3 better,1/3 same, 1/3 ESRF• Idiopathic, or assoc Malignancy, drugs, SLE (V), Hep B

Nephrotic syndrome

• Other causes of Nephrotic syndrome:

– Focal Segmental Glomerulosclerosis• Only some (focal) glomeruli have some (segmental)

sclerosis. Idiopathic or assoc HIV• High recurrence in transplant

– DM– Amyloid– SLE

Nephritic Syndrome

• Symptomatic haematuria and proteinuria

– Haematuria with red cell casts– Proteinuria (<3.5g/day)– Oliguria– Hypertension– Oedema

– (remember UTI can give you haematuria and proteinuria)

Nephritic Syndrome

• Commonest cause:– IgA nephropathy (Bergers disease)

• 3-4 days post infection – usually URTI• 16-35 yr olds with episodic macroscopic haematuria• IgA and C3 on biopsy with mesangial hypercellularity

• 2nd commonest:– Proliferative GN / Post Strep GN – 1-3 weeks post strep infection

• IgG and C3 on biopsy• ASOT (anti streptolysin-O-Titre)

Nephritic syndrome

• Other causes:– HSP (Henoch Schonlein Purpura)

• Systemic variant of IgA nephropathy• Usually 3-10yrs old

– Plus fever, rash (purpura on legs and buttocks), joint pain, abdo pain

– SLE– Cryoglobulinaemia– Infective endocarditis– Tubulointerstitial nephritis

Asymptomatic haematuria and proteinuria

• Alports syndrome – (inherited renal failure and deafness)

• Thin basement membrane disease– (inherited AD, BP and renal function normal)

• Remember UTI– But often plus frequency, dysuria, temperature

Parts of Kidney

• Simplified– Glomerulus– Blood vessels– Tubules– Interstitium

Glomerulonephritis

• Inflammation of glomerulus

• Usually present with:– Haematuria with red cell casts– +/- Proteinuria

– May present as ARF, nephritic or nephrotic syndrome

GN• IgA (bergers disease)

– IgA, young girl, 3-4 days post URTI• Minimal change

– Commonest cause of nephrotic syndrome in kids, fusion of podocytes, treat high dose Prednisolone, excellent prognosis

• Membranous– Commonest cause of nephrotic syndrome in adults, thickened BM with spikes

(IgG), idiopathic, or malignancy, SLE, Drugs or Hep B• Proliferative (post strep)

– Post Strep, 1-3 weeks post infection, IgG on biopsy, ASOT and low C3• Focal Segmental Glomerulosclerosis

– Only some glomeruli have segmental sclerosis, assoc HIV, high recurrence in transplants

• Thin BM disease– AD – family history, heamaturia without renal failure or hypertension

GN• Membranoproliferative/mesangiocapillary

– Mesangial proliferation with double BM– Two types

• I - assoc Cryoglobulinaemia/Hepatitis C• II - assoc Partial lipodystophy

• Rapidly progressive GN– ESRF in weeks– Focal necrotising GN with cresentic changes– Assoc:

• Vasculitis – Wegners/Churg-Strauss• Goodpastures• SLE/ RA• Other GN (eg IgA)

Parts of kidney

– Glomerulus– Blood vessels– Tubules– Interstitium

Act as one

Tubulointerstitial Nephritis• A cause of a Nephritic type picture due to damage to

the tubules or interstitium

• Almost all due to hypersensitivity reactions to drugs– Penicillins or NSAIDS

– Also Cadmodium, mercury, reflux, sickle cell or urate nephropathy

• Often get Eosinophilia• May have fever, arthralgia and rash• ‘Non-oliguric renal failure’• (No red cell casts – signifies glomerular

damage)

Renal Failure

Acute Renal FailureChronic renal failure

Acute renal failure

• Suddenly and usually reversible loss in renal function occurring over hours or days.

• Usually associated with a reduced urine volume

Causes ARF– Pre-renal - Decreased perfusion of kidneys

• shock/hypovolaemia• (usually reversible but may progress to ATN)

– Renal• ATN(85%)• GN/interstitial disease

– Post renal - Obstruction of urine flow• Intra-lumen – stone• In the wall – stricture/tumour• Compressing wall – prostate/tumour/AAA

• Remember blocked catheter if catherised

Acute tubular necrosis - ATN

• Tubular cells have a very high oxygen requirement.

• If deprived of oxygen they die• Take 7-21 days to regenerate• If insult is prolonged the damage may be

irreversible

• Oliguria – polyuria - normal

Uraemia• (a term loosely applied to describe the symptoms that accompany renal

failure, presumably due to build up of toxic products)

• Anorexia, nausea, vomiting• Pruritis, hiccups• Encephalopathy, fits, coma

• Pulmonary oedema, hyperkalaemia, acidosis

Approach to ARF

• Rule out or treat hypovolaemia• Insert catheter (rules out obstruction and allows

close monitoring of fluid balance)• Urine dip• Bloods (U&Es, FBC, ABG, ECG, CRP (+/-ANA, anti GBM, ANCA))

• USS urinary tract• Early nephrological advice• Treat complication – e.g. hyperkalaemia, adjust drug

doses e.g. gentamicin

Dialysis in ARF

• 4 main indications

– Hyperkalaemia not responding to medical treatment

– Pulmonary oedema not responding to medical treatment

– Severe acidosis– Complications of uraemia – pericarditis or

encephalopathy

Chronic Renal Failure

• Substantial and irreversible deterioration of renal function, classically develops over a period of years

• Commonest causes– DM– HTN– Glomerulonephritis– ADPKD

Chronic renal failure - Problems

• Fluid retention• Anaemia (Burr cell)• Metabolic bone disease

– (low Ca, high phosphate)– Hyperparathyroidism (2 and 3rd), osteomalacia, osteoporosis

• Infection• Hypertension, increased CVS risk• Pericarditis (uraemic)• Acidosis, hyperkalemia

Approach to CRF

• Identify cause• Prevent further progression if possible

• Once creatinine hits 300 there is usually progressive deterioration regardless of the cause

Dialysis in CRF

• This should be started when patient has advanced renal failure, but before they develop complications

• Usually creatinine around 600-800• Usually haemodialysis 4 hours 3x a week

Dialysis• 2 main types

• Intermittent haemodialysis– AV fistula– Better filtration

• Continuous peritoneal dialysis– ‘Tenckhoff’ catheter– Better kids (growth) and elderly (less haemodynamic

fluctuations)

• (Haemofiltration – ITU, continuous)

Transplant

• Refer to transplant team early• Transplant nurse, transplant coordinator etc• Needs ABO and HLA compatibility

• 90%1 year graft survival• 50% 10 year graft survival

• Best with living related donor

Transplant drugs

• Steriods• Azathioprine• Ciclosporin• Tacrolimus/Sirolimus• Mycophenolate

Complication of transplant

• Graft failure– Acute – usually preventable with

immunosuppressant's– Chronic – Slow decline in function – irreversible

• Infection• Malignancy – skin (SCC), lymphoma• Side effects of drugs – e.g. gum hypertrophy

with ciclosporin

Diseases which can reoccur in a graft

• IgA Nephropathy• Goodpastures• Focal Segmental Glomerulosclerosis• Metabolic diseases (DM)

Rare Renal

Goodpastures

• Autoantibodies against type IV collagen in lung and kidney basement membrane (anti –GBM)

– Haemoptysis– Haematuira

• Immunosuppression and plasma exchange (recurs in transplant)

Wegners

• A vasculitis with granulomas

• Get sinusitis, nose bleeds, nasal deformities, arthritis, cavitating lung lesions, haemoptysis and renal failure

• Circulating C-ANCA against PR3

SLE and Scleroderma

• Kidneys often involved

• No renal involvement in drug induced SLE

• SLE renal involvement graded I-V, V being nephrotic syndrome due to membranous GN

• Scleroderma can get renal crisis – ACEi and dialysis can be lifesaving

DM

• Diabetics often have kidney damage• It is a microvascular complication

– (due to ischemia, glycosilation)

• Get Kimmelstiel-Wilson nodules in kidneys• Microalbuminuria (30-300) is one of the first

signs – is screened for• ACEi is renoprotective

Tumour Lysis Syndrome

• When cells die they release contents into blood

• When large number of cells die all at once, often in cancer on starting treatment urate levels begin to cause issues

• Urate causes ARF• Oncologists often start allopurinol (or

Rasburicase) prior to chemotherapy

ADPKD

• Autosomal dominant polycystic renal disease• PKD1 (chromo 16) PKD2 (chromo 4)• Multiple cysts in kidneys cause:

– Enlargement– Pain– Haematuria– Renal failure– At risk of SAH

• Screen with USS

Multiple Myeloma

• ARF is common in myeloma– Immunoglobulins can block tubules – get

‘fractured casts with giant cell reaction’– At risk of infection– High calcium damages kidney

Renal Tubular Acidosis

• Rare cause of metabolic acidosis due to renal issues

• “If patient is acidotic and urine is not the suspect”

RTA• Type I

– Don’t get rid of H+ in distal tubule– Assoc stones and hypokalaemia

• Type II– Leak bicarbonate– No stones, usually assoc fanconi’s syndrome

• Type IV– Get Hyperkalaemia– Usually in diabetics with mild renal failure

Fanconi syndrome

• Generalised disturbance of renal function• Can be inherited or acquired• A cause of RTA II

Hepatorenal Failure

• Renal failure as a consequence of liver failure• Very poor prognosis unless liver sorted out

Amyloid

• ‘Extracellular deposition of protein which form B-pleated sheets’

• Tissues/organs become larger and firmer• On microscopy get ‘apple green birefringence

in polarized light after staining with congo-red’

• Often due to myeloma (AL) or chronic inlammatory diseases (AA)

• Can cause renal failure

Renal artery stenosis

• A cause of hypertension• Narrowing in artery to kidney (e.g.

athersclerosis, NF) decreases perfusion pressure

• That kidney begins to increase blood pressure (renin-angiotensin-aldosterone)

• Get asymetrical kidneys on USS• ACEi are contraindicated

UTI

UTI• Mostly E-Coli (70% E-coli)

– Can use • Trimethoprium• Nitrofurantoin• Amoxicillin• (Cefalexin a favourite if pregnant)

– Three day course if uncomplicated

• If developed pyelonephritis – needs i.v antibiotics (renal angle tenderness, rigors)

• Staph Saprophiticus – UTI only• Proteus – staghorn calculi• Pseudomonas – long term catheter, green

UTI

• Remember STIs as a cause of dysuria• Can get sterile urethritis• Can get asymptomatic Bacteriuria – treat if

pregnant• If suspect TB do three EMU• Prostate can be infected perianal pain and

tender prostate, difficult to treat, long course of Abx

Pyelonephritis

• Infection of the kidney• Usually due to ascending infection

• Fever/Rigors• Loin pain

• Needs admisison, treat often with gentamicin, cephalosporin or ciprofloxacin

Renal stones (nephrolithiasis)

• Pain – loin to groin, can’t get comfortable, rolling around

• 95% have haematuria on dipstix• Commonest cause: Calcium oxalate,• Others: triple phosphate (staghorn calculi),

uric acid (radio lucent)

• Risk factors – dehydration, UTI, hypercalcaemia, high dietary oxalate

Renal stones

• Treat:– Diclofenac, esp PR is excellent– May need antiemetic

• Check U&Es to ensure no renal failure from obstruction• Do X-ray KUB, IVU or CT KUB• Often pass on their own can do lithrotripsy, esp for

renal pelvis

• (Don’t forget AAA as a cause of ‘renal colic’)

BPH

• Benign prostatic hyperplasia• Protate gets uniformly enlarged – smooth on

pr• PSA may be slightly raised• May get symptoms of Bladder outflow

obstruction– Hesitancy, poor stream, terminal dribbling,

nocturia

BPH

• Treatment– Drugs

• Tamsulosin – a-blocker relaxes smooth muscle particular in urogenital tract and eases some of the outflow obstruction

• Finasteride – 5a blocker, interfers with testosterone conversion to potent DHT, helps provent progression

– Surgery• TURP – Transurethral resection of the prostate

Prostate cancer

• 2nd commonest malignancy of men• Adenocacinoma that arises in peripheral

prostate• PSA tumour marker• Likes metasisizing to bone (sclerotic lesions on

x-ray)

Prostate cancer• Craggy prostate on PR• Raised PSA (>4ug/l)• Do Transrectal ultrasound and biopsy• Bone scan/CT/MRI pelvis

• Gleason score – two scores 1-5– Min score 2 max 10

• Treat Prostatectomy/Radiotherapy/Brachytherapy/Chemotherapy (Zolodex)Watch and wait

Torsion

• Urological emergency– Testis twists and cuts off blood supply– Will die in hours– Sudden onset of pain– Testis may lie high and transversely

– Needs surgery – untwist and if viable do orchidoplexy, if not ochidectomy

Testicular lumps

• Can you get above it – ie is it a hernia

• Cold, hard, attached to testis – Cancer• Whole testis swollen and tender – Epididymo-

orchitis• Is it a lumpy ‘bag of worms’ ontop – varicocele• Is it cystic – above testis – epididymal cyst• Is it cystic – surrounds testis - hydrocele

Testicular tumours

• Painless hard lump on testis

• Germ cell– Teratomas, 20-30s, secrete BHCG and aFP– Seminomas, 30-40s, secrete alk phos

• Treat Orchidectomy and chemo – esp cisplatin

• Non germ cell– Leydig, sertoli and lymphoma

RCC• Renal cell carcinoma, aka clear cell• Classic triad of

– Pain– Haematuria– Renal mass

• Assoc smoking and von Hippel Lindau• Can spread via direct extension, blood and lymph. • Have a special ability to grow along vessels renal vein

to IVC• Can secrete EPO

TCC

• Transitional cell carcinoma• Can arise from Bladder, Ureter or renal pelvis• Assoc smoking and analine dies

• Think in anyone >50 with painless haematuria• Can do urine cytology, often do cystoscopy

• Schistosomiasis can cause SCC of the bladder

Paeds Urology

• Phimosis – narrowing of opening of foreskin• Paraphimosis – swelling of glans due to tight

foreskin being retracted and not replaced• Hypospadias – abnormal opening of urethra• Undescended testis – common in prems, try

to surgically correct, if intra-abdominal remove due to risk of malignant change

• Balanitis – inflammation of the glans

Notes

• Hyaline casts in normal individuals• Granular casts in renal damage• Dysmorphic RBCs indicate glomerular disease• Destruction of capillary loops – vasculitis• Tubular atrophy - CRF