Glomerulonephritis

DEFINITION

 Glomerulonephritis is immunologically mediated inflammation of renal glomeruli.

AETIOLOGY

There are many different types of glomerulonephritis with differing aetiologies. Some types of glomerulonephritis are ascribed to deposition of antigen–antibody immune complexes in the glomeruli that lead to inflammation and activation of complement and coagulation cascades. The immune complexes may either form within the glomerulus (more commonly) or be deposited from the circulation. The antigens in the immune complexes are often unknown but may occasionally be associated with the following:

Infection: Bacterial: Streptococcus viridans, group A b-haemolytic streptococci, staphylococci, gonococci, Salmonella, syphilis.

Viral: Hepatitis B/C, HIV, measles, mumps, EBV, VZV, coxsackie.

Protozoal: Plasmodium malariae, schistosomiasis, filariasis.

Inflammatory/systemic diseases: SLE, systemic vasculitis, cryoglobulinaemia.

Drugs: Gold, penicillamine.

Tumours:

Classified based on the site of nephron pathology and its distribution.

Minimal-change glomerulonephritis: Normal appearance on light microscopy. Electron microscopy: Loss of epithelial foot processes.

Membranous glomerulonephritis: Thickening of GBM from immune complex deposition.Associated with Goodpasture’s syndrome.

Membranoproliferative glomerulonephritis (MPGN): Thickening of GBM, mesangial cell proliferation and interposition.

Type 1: Subendothelial immune complex deposits and reduplication of GBM.

Type 2: Dense intramembranous deposits (stain only for C3).

Focal segmental glomerulosclerosis: Glomerular scarring. Associated with HIV.

Focal segmental proliferative glomerulonephritis: Mesangial and endothelial cell proliferation. ‘Focal’ refers to involvement of some of the glomeruli, ‘segmental’ refers to involvement of parts of individual glomeruli.

Diffuse proliferative glomerulonephritis: Same as above but affects all glomeruli.

IgA nephropathy: Mesangial cell proliferation and mesangial IgA and C3 deposits.

Crescentric glomerulonephritis: Crescent formation by macrophages and epithelial cells,which fills up Bowman’s space.

Focal segmental necrotizing glomerulonephritis: Peripheral capillary loop necrosis (e.g. in Wegener’s granulomatosis, microscopic polyarteritis and other vasculitides). Often evolves into crescentric glomerulonephritis.

EPIDEMIOLOGY

 Makes up to 25% of cases of chronic renal failure.

HISTORY

 Haematuria, subcutaneous oedema, polyuria or oliguria, proteinuria. History of recent infection.

Symptoms of uraemia or renal failure (acute and chronic).

Cryoglobulins are immunoglobulins that precipitate in cold, and may be monoclonal or polyclonal. They can cause cutaneous vasculitis.

Goodpasture’s syndrome result from anti-GBM antibody that binds to an antigen in the basement membrane. The antibody also reacts with pulmonary capillary basement membrane and can cause pulmonary haemorrhage.

 

EXAMINATION

 May present with the signs of the following:

• . hypertension;
• . proteinuria (<3 g/24 h);
• . haematuria (microscopic or macroscopic, especially IgA nephropathy);
• . nephrotic syndrome (usually for minimal-change glomerulonephritis in children and membranous glomerulonephritis in adults; see nephrotic syndrome);
• . nephritic syndrome (haematuria, proteinuria, subcutaneous oedema, oliguria, hypertension, uraemia);
• . renal failure (acute or chronic); and
• . partial lipodystrophy (loss of subcutaneous fat in MPGN type II).

INVESTIGATIONS

Blood:

 FBC, U&E and creatinine, LFT (albumin), lipid profile, complement studies (C3, C4, C3 nephritic factor in MPGN), ANA, anti-double stranded DNA,ANCA, anti-GBM antibody, cryoglobulins if appropriate.

Urine:

 Microscopy (dysmorphic RBCs, red-cell casts), 24-h collection: creatinine clearance,protein.

Imaging:

 Renal tract ultrasound (to exclude other pathology).

Renal biopsy: 

Light microscopy, electron microscopy, immunofluorescence microscopy.

Investigations for associated infections: 

e.g. hepatitis B, hepatitis C or HIV serology.

MANAGEMENT

 Fluid balance:

 Monitor input/output and weight changes, avoid added salt and restrict fluid if there are signs of fluid overload or " BP.

Treatment of complications:

 (see hypertension; renal failure, acute; renal failure, chronic,nephrotic syndrome).

Focal necrotizing glomerulonephritis, rapidly progressive crescentric glomerulonephritis,glomerulonephritis associated with SLE, primary vasculitides: Steroids, azathioprine,ciclosporin A, cyclophosphamide.

Consider plasma exchange, especially for severe disease affecting the basement membrane.

COMPLICATIONS

Pulmonary oedema: " Risk of hypertension, hypertensive encephalopathy. Renal failure. Complications of nephrotic syndrome. Pre-eclampsia in pregnancy.

PROGNOSIS

 Minimal-change glomerulonephritis and post-infective diffuse proliferative glomerulonephritis mostly resolve.

Risk of CRF: Focal segmental sclerosis 50–75%; focal proliferative glomerulonephritis 25%; membranous glomerulonephritis 30%; MPGN >75%.

Poor prognostic factors: " Creatinine when first seen, " BP, persistent proteinuria.

0 تعليق

PH.Jafar Jassim 12/24/2020 01:02:00 ص

تابع القراءه

Renal artery stenosis

D E F I N I T I ON

 Stenosis of the renal artery.

AET IOLOGY 

Main cause:

. Atherosclerosis (older patient): Widespread aortic disease involving the renal artery ostia.

. Fibromuscular dysplasia (younger patient): Fibromuscular dysplasia is of unknown aetiology

but may be associated with collagen disorders, neurofibromatosis and Takayasu’s

disease. This may be associated with micro-aneurysms in the mid and distal renal arteries

(resembling string of beads on angiography).

E P IDEMI OLOGY 

Prevalence is unknown but believed to account for 1–5% of all hypertension;

fibromuscular dysplasia occurs mainly in women with hypertension at <45 years.

H ISTORY 

History of hypertension in <50 years.

Hypertension refractory to treatment.

Accelerated hypertension and renal deterioration on starting ACE inhibitor.

History of flash pulmonary oedema.

EXAMI N A T ION

Hypertension.

Signs of renal failure in advanced bilateral disease.

An abdominal bruit may be heard over the stenosed artery.

PATHOLOGY/PATHOGENESI S

 Renal hypoperfusion stimulates the renin-angiotensin

system leading to " circulating angiotensin II and aldosterone, increasing BP, which in

turn, with time, causes fibrosis, glomerosclerosis and renal failure.

I N V E S T IGATIONS

 Non-invasive: Duplex ultrasound (technically difficult if obese). Ultrasound

measurement of kidney size (predicts outcome after revascularization, kidneys

<8 cm are unlikely to improve).

CT angiography or MRA: Often used now; risk of contrast nephrotoxicity.

Digital subtraction angiography: Gold standard assessment.

Renal scintigraphy: Uses the radio-agent 99Tc-DTPA (excreted by glomerular filtration) or

99Tc -MAG3 (excreted by tubules). Addition of an ACE inhibitor (captopril

renography) causes delayed clearance by the affected kidney (may not be helpful if

bilateral RAS).

MANAGEMENT

 Medical: Pharmacological control of hypertension. In atherosclerotic

cases, medical treatment is often preferred together with modulation of other cardiovascular

risk factors. Avoidance of ACE inhibitors and other nephrotoxic agents.

Intervention: In cases of uncontrolled hypertension, progressive renal failure, flash pulmonary

oedema, stenoses >60%.

Angioplasty þ/stenting: Treatment of choice for fibromuscular dysplasia, less effective in

atherosclerotic cases.

Surgical revascularisation: Several approaches are used, e.g. aortorenal bypass using saphenous

vein or synthetic grafts (PTFE or Dacron), aortic replacement and renal reconstruction,

endarterectomy of atherosclerotic RAS, extra-anatomical bypass (hepatorenal on

right, splenorenal on left).

COMPL I C A T IONS 

Drug-refractory hypertension, renal failure.

Of angioplasty: Restenosis (occurs in up to 20%), rarely renal artery rupture or thrombotic

occlusion may require emergency surgery (with high mortality 40%).

P ROGNOS I S

 Untreated hypertension will progress to renal failure. With intervention

50–70% will have improvement in BP and renal function. Curative in 15%.

0 تعليق

PH.Jafar Jassim 12/22/2020 10:47:00 م

تابع القراءه

Renal calculi

D E FI N I T ION

 Different types include calcium oxalate (65%), calcium phosphate (15%)

magnesium ammonium phosphate (10–15%), uric acid (2–5%), cystine (1%)1.

AE T IOLOGY 

Commonly idiopathic or caused by dehydration or urinary tract infections.

Other risk factors are:

Changes in urinary pH: Calcium oxalate, calcium phosphate and magnesium ammonium

phosphate stones arise in alkaline urine, cystine and uric acid stones arise in acid urine.

Hypercalciuria: Usually idiopathic, drug (lithium, thiazides).

Hypercalcaemia: Malignancy, hyperparathyroidism, sarcoidosis, myeloma, " calcium intake

(‘milk-alkali syndrome’).

Hyperoxaluria: Causes: " intake (in rhubarb, spinach, strawberries, tea, tomatoes, beetroots,

beans, chocolate, nuts), " colonic absorption in patients with small bowel disease or

resection, autosomally recessive inherited enzyme deficiency ! " oxalate production

and excretion.

Hyperuricaemia: Tumour lysis syndrome, high cell turnover states.

Cystinuria: Autosomal recessive, defect of renal tubular transport of cystine and dibasic amino

acids.

Anatomical anomalies: e.g. horseshoe kidneys.

E P IDEMIOLOGY

 UK prevalence 2%, lifetime incidence up to 12%. Peak age of presentation

20–50 years. <: ,  2:1.

H ISTORY AND EXAMI N A T I ON 

May be asymptomatic.

Pain: Loin pain (kidney stones). Renal colic radiating from loin ! groin, scrotum, labium

(ureteric stones). Dysuria, frequency, strangury, penile tip pain (bladder stones). Urinary

retention and bladder distension (urethral stones).

Haematuria.

Symptoms of urinary tract infection and obstruction.

INVE S T I G A T IONS 

Blood: U&E, calcium, phosphate, albumin.

PTH, vitamin D, urate, bicarbonate, serum ACE, thyroid function.

Urine: Urinalysis (blood, protein, nitrites), microscopy and culture. 24-h collection: creatinine

clearance, calcium, phosphate, oxalate and urate. Random urine for cystine, glyoxolate,

citrate.

Plain radiography (‘KUB’): Shows radio-opaque stones (calcium oxalate stones are radioopaque,

cystine stones are semi-opaque, urate stones are radio-lucent).

Intravenous urograpm (IVU): IV contrast followed by radiographs may show a filling defect in

the urinary outflow.

High resolution helical CT-abdomen: High diagnostic accuracy and can visualise radio-lucent

calculi.

Renal ultrasound: To assess for hydronephrosis or hydroureter.

Chemical analysis of the stone: If passed.

1Appearances of renal calculi depend on composition:

Calcium oxalate: ‘Mulberry’ stones with spiky surface, dark (covered by blood from the mucosa of the renal

pelvis injured by the sharp projections).

Calcium phosphate and magnesium ammonium phosphate: Smooth, may be large and take the shape of

calyces. ‘Staghorn’ calculi, dirty white.

Uric acid: Hard, smooth, faceted, yellow/light brown. These are radiolucent.

Cystine: Translucent, white.

Renal calculi (continued)

MANAGEMENT 

Medical Expulsive Treatment: Suitable for <10mm calculi.

Opiate and NSAID analgesics.

Rehydration (Oral or IV).

Treat exarcebtaing factors and UTI.

Calcium channel antagonists (e.g. nifedipine) reduce ureteric spasm.

Alpha-antagonists (e.g. tamsulosin) reduce ureteric spasm.

Extracorporeal shockwave lithotripsy (ESWL): Provides non-invasive outpatient treatment and

usually combined with medical treatment. Usually suitable for smaller stones in the

kidneys or ureter.

Cystoscopy: allows visualization of the stone and urinary tract as well as laser to break up the

stone.

Percutaneous nephrolithotomy: May be necessary for calculi >2 cm or not suitable for other

modalities.

Prevention: " Fluid intake (e.g. >3 L/day avoiding high Ca2þ

water).

Calcium stones: # calcium and vitamin D intake.

Oxalate stones: # oxalate-containing foods and vitamin C intake.

Uric acid stones: Allopurinol (inhibits xanthine oxidase and uric acid synthesis), urinary

alkalization (oral sodium bicarbonate).

Cystine stones: D-penicillamine, urinary alkalinization.

COMPL I C A T IONS

 Obstruction and hydronephrosis, infection, complications of the cause,

e.g. renal failure in primary hyperoxaluria.

P ROGNOS I S 

Approximately 20% of calculi will not pass spontaneously. Up to 50% of

patients may have recurrence within 5 years.

0 تعليق

PH.Jafar Jassim 12/22/2020 10:39:00 م

تابع القراءه

Nephrotic syndrome

D E FI N I T ION 

Characterized by proteinuria (>3 g/24 h), hypoalbuminaemia (<30 g/L),

oedema and hypercholesterolaemia.

AE T IOLOGY 

Commonest cause is minimal change glomerulonephritis in children, but all

forms of glomerulonephritis can cause nephrotic syndrome.

Other causes: Diabetes mellitus, sickle cell disease, amyloidosis, malignancies (lung and GI

adenocarcinomas), drugs (NSAIDs), Alport’s syndrome, HIV infection.

E P IDEMIOLOGY 

Most common cause of nephrotic syndrome in children (90%): minimal

change glomerulonephritis (usually seen in boys <5 years, rare in black populations).

Most common causes of nephrotic syndrome in adults: diabetes mellitus, membranous

glomerulonephritis.

H ISTORY

 Family history of atopy in those with minimal change glomerulonephritis, family

history of renal disease.

Swelling of face, abdomen, limbs, genitalia.

Symptoms of the underlying cause (e.g. SLE).

Symptoms of complications (e.g. renal vein thrombosis: loin pain, haematuria).

EXAMINA T I ON 

Oedema: Periorbital, peripheral, genital.

Ascites: Fluid thrill, shifting dullness.

PATHOLOGY/PATHOGENESI S

 Structural damage to the basement membrane or the

reduction in the negatively charged components within it reduces the filtration of large

protein molecules by the glomerulus, causing proteinuria and hypoalbuminaemia.

INVE S T I G A T IONS 

Blood: FBC, U&E, LFT (# albumin), ESR/CRP, glucose, lipid profile

(secondary hyperlipidaemia), immunoglobulins, complement (C3, C4).

Tests to identify the underlying cause of glomerulonephritis:

SLE: ANA, anti-dsDNA.

Infections: Group A b-haemolytic streptococcal infection (ASO titre), HBV infection (serology),

plasmodium malariae (blood films).

Goodpasture’s syndrome: Anti-glomerular basement membrane antibodies.

Vasculitides: e.g. Wegener’s and microscopic polyarteritis (ANCA).

Urine: Urinalysis (protein, blood), microscopy, culture, sensitivity, 24-h collection (to calculate

creatinine clearance and 24-h protein excretion).

Renal ultrasound: Excludes other renal diseases that may cause proteinuria, e.g. reflux

nephropathy.

Renal biopsy: In all adults and in children who have unusual features or do not respond to

steroids.

Other imaging: Doppler ultrasound, renal angiogram, CT or MRI are options if renal vein

thrombosis is suspected.

MANAGEMENT 

Treat oedema:

. Fluid restriction (1 L/day),

. Naþ restriction (50 mmol/day),

. diuretics (e.g. oral furosemidemetolazone or spironolactone),

. occasionally, IV diuretics and salt-poor albumin may be required for initiation of diuresis.

Treat the cause:

. Minimal change glomerulonephritis: High-dose steroids (60mgfor 2months) and gradually

# the dose, treat relapses (40% within 3 years) with steroids, immunosuppressants:

cyclophosphamide or ciclosporin for steroid non-responders or those with relapses.

. Membranous glomerulonephritis: The benefit of steroids and immunosuppressants is

uncertain.

. SLE: Corticoteroids, cyclophosphamide.

NEPHROLOGY

 123

Nephrotic syndrome (continued)

Monitor:

. BP, U&E, weight, fluid balance.

. Thromboprophylaxis: Heparin.

COMPL I C A T IONS 

Renal failure (caused by hypovolaemia especially following diuretics,

renal vein thrombosis, progression of underlying renal disease), " susceptibility to infection

(e.g. peritonitis, pneumococcal because of loss of immunoglobulins and lipid content in the

urine), thrombosis (e.g. renal vein and DVT caused by hypovolaemia and hypercoagulable

state caused by loss of antithrombin in the urine and " synthesis of fibrinogen in the liver),

hyperlipidaemia (possibly caused by " synthesis of trigylcerides and cholesterol along with

albumin in the liver).

P ROGNOS I S 

Varies according to the underlying condition and presence of complications

0 تعليق

PH.Jafar Jassim 12/15/2020 11:26:00 م

تابع القراءه

Renal failure (acute)

D E FI N I T ION 

Impairment of renal function over days or weeks, which often results in "

plasma urea/creatinine and oliguria (<400 mL/day) and is usually reversible. The term acute

kidney injury (AKI) represents the full spectrum of acute kidney dysfunction.

AE T IOLOGY Pre-renal (# renal perfusion):

Shock (hypovolaemic, septic, cardiogenic), hepatorenal syndrome (liver failure).

Renal:

Acute tubular necrosis (ATN): Ischaemia, drugs and toxins (paracetamol, aminoglycosides,

amphotericin B, NSAIDs, ACE-inhibtors, lithium).

Acute glomerulonephritis.

Acute interstitial nephritis: NSAIDs, penicillins, sulphonamides, leptospirosis.

Small or large vessel obstruction: Renal artery/vein thrombosis, cholesterol emboli, vasculitis,

haemolytic microangipathy (e.g. HUS or TTP).

Others: Light-chain (myeloma), urate (lympho- or myeloproliferative disorders, particularly

after chemotherapy/radiation induced cell lysis), pigment (haemolysis, rhabdomyolysis,

malaria) nephropathy, accelerated phase hypertension (e.g. in pre-eclampsia).

Post-renal: Stone, tumour (pelvic, prostate, bladder), blood clots, retroperitoneal fibrosis.

E P IDEMIOLOGY

 A population-based study estimates an incidence of 1800 per million.

H ISTORY 

Malaise, anorexia, nausea, vomiting, pruritus, drowsiness, convulsions, coma

(caused by uraemia). Symptoms of the cause or complications usually dominate (see below).

EXAMINA T I ON 

Oedema, signs of the cause and complications (see below).

INVE S T I G A T IONS 

Blood: ABG, FBC, U&E (urea, creatinine, Na

þ

, K

þ

), LFT, ESR/CRP,

Ca2þ

, clotting, culture, blood film: red cell fragmentation in HUS/TTP.

Other blood tests: CK (for rhabdomyolysis), urate, serum electrophoresis and autoantibodies.

Urine:Stick testing: Haematuria, proteinuria (e.g. glomerulonephritis).

Microscopy: Red cell casts (in glomerulonephritis). Culture and sensitivity. Bence-Jones

protein (exclude myeloma). Urine osmolality/Naþ

:

. Renal ARF: # Urine osmolality/specific gravity (as a result of # renal concentrating ability), "

urine Na

þ

(as a result of # reabsorptive ability), " fractional excretion of Na

þ

(PCr.UNa/

PNa.UCr): >2%.

. Pre-renal ARF: " Urine osmolality, # urine Na

þ

, # fractional excretion of Na

þ

(<1%).

CXR: To monitor for fluid overload.

ECG: Check for hyperkalaemia (tented T waves).

Renal ultrasound: To exclude an obstructive cause.

Renal biopsy (e.g. acute tubulointerstitial nephritis: tubulitis and intense interstitial cellular

infiltrate including eosinophils).

MANAGEMENT 

Assess hydration and fluid balance: Pulse rate, lying and standing BP, JVP,

skin turgor, chest auscultation, ?peripheral oedema, CVP, fluid and weight charts.

Treat the complications:

Hyperkalaemia (if ECG changes or K

þ

>7 mmol/L):

. 10 mL of 10% calcium gluconate IV (protect the myocardium) and ECG monitoring.

. 50 mL 50% dextrose with 5U actrapid insulin over 15 min (drive K

þ

into cells).

. Nebulized salbutamol can also # K

þ

.

. Ca2þ

/Na

þ

resonium PO/PR (# bowel absorption).

. Contact renal team and arrange for dialysis if appropriate (see below).

Metabolic acidosis (if pH<7.2):

. 50–100 mL of 8.4% bicarbonate via central line over 15–30 min.

Pulmonary oedema:

. O2, consider CPAP.

. IV GTN 2–10 mg/h.

NEPHROLOGY

 129

Renal failure (acute) (continued)

. IV furosemide: 250mg over 1 h, followed by infusion (5–10 mg/h).

. IV diamorphine (single dose of 2.5 mg) relieves anxiety and breathlessness.

Treat the cause:

. IV fluids if volume depleted: 500 mL colloid or 0.9% saline over 30 min, assess response

(i.e. urine output/CVP), continue fluids until CVP 5–10 cm. Inotropes if hypotension

persists in spite of CVP of >10 cm.

. Treatment of infection: adjust the dose of antibiotics in view of the renal impairment.

. Stop the nephrotoxic drugs (e.g. ACEI and NSAIDs) and non-essential drugs.

. Identify intrinsic renal disease and treat.

. Relieve the obstruction e.g. urinary catheter, nephrostomies.

Optimize nutritional support.

Identify and treat bleeding tendency: Prophylaxis with PPIs or H2 antagonist, transfuse if

required, avoid aspirin.

Indications for haemofiltration/dialysis (see below): Persistent hyperkalaemia (K

þ

>7 mmol/

L), fluid overload (e.g. refractory pulmonary oedema), pericarditis, acidosis (arterial

pH<7.1, bicarbonate <12 mmol/L), symptomatic uraemia (tremor, cognitive impairment,

coma, fits, urea typically >45 mmol/L).

Haemofiltration (continuous arteriovenous or venous–venous): Filtration of plasma water

across the membrane induced by the hydrostatic pressure gradient, and ‘convective’

transport of solutes in the same direction as water. Substitution fluid is required to prevent

excessive fluid removal.

Dialysis: Intermittent haemodialysis (using central venous catheters or arteriovenous fistulae)

or peritoneal dialysis (using a double cuff straight Tenckhoff catheter). Solutes passively

diffuse down their concentration gradient (urea, creatinine and potassium move from

blood to dialysate, calcium and bicarbonate, move from dialysate to blood).

Venesect 250–500 mL if delay for dialysis.

The choice of modality depends upon: availability, expertise, haemodynamic stability,

vascular access, and whether the primary need is for fluid and/or solute removal.

Haemofiltration is preferred in hypotensive or haemodynamically unstable patients since

the rate of fluid and solute removal is slow.

Treatment of pigment/light chain/urate nephropathy

Pigment nephropathy: Isotonic saline to maintain diuresis of 200–300 mL/h. Careful

monitoring for fluid overload. If a diuresis is established, switch to an alkaline solution

(bicarbonate). " Urine pH to >6.5 may # release of free iron from myoglobin and

intratubular pigment deposition and cast formation. If the desired diuresis is not

establishedwith adequate volume repletion alone: loop diuretics or mannitol (if mannitol

is used, monitor plasma osmolality).

Myeloma cast nephropathy: Thalidomide and dexamethasone to # light chain production.

Isotonic fluids (aim urine output 3 L/day), careful monitoring for fluid overload.

Urate nephropathy: Allopurinol, loop diuretic and fluids (to wash out the obstructing uric acid

crystals). Haemodialysis if diuresis cannot be induced.

COMPL I C A T IONS

 Common and life-threatening: Hyperkalaemia, sepsis, metabolic acidosis,

pulmonary oedema, hypertension.

Less common: Gastric ulceration, bleeding (platelet dysfunction), muscle wasting (hypercatabolic

state), uraemic pericarditis, uraemic encephalopathy, acute cortical necrosis.

P ROGNOS I S ATN

 has biphasic recovery starting with oliguria then leading to polyuria

(resulting from regeneration of the tubular cells). Prognosis depends on the number of other

organs involved, e.g. heart, lung. Many of those with ATN recover. Acute cortical necrosis

may cause hypertension and chronic renal failure

0 تعليق

PH.Jafar Jassim 12/15/2020 11:14:00 م

تابع القراءه

Renal failure (chronic)

D E FI N I T ION 

Chronic renal failure or chronic kidney disease (CKD) is defined as either

kidney damage or GFR <60 mL/min/1.73m2 for 3 months. Kidney damage is defined as

pathologic abnormalities or markers of damage, including abnormalities in blood or urine

tests or imaging studies.

Stage GFR (mL/min/1.73m2)

1 90

2 60–89

3 30–59

4 15–29

5 <15

AE T IOLOGY

 Diabetes mellitus and hypertension are the two most common causes.

Vascular disease: Hypertension, renal artery atheroma, vasculitis.

Glomerular disease: Glomerulonephritis, diabetes, amyloid, SLE.

Tubulointerstitial disease: Pyelonephritis/interstitial nephritis, nephrocalcinosis, tuberculosis.

Obstruction and others: Myeloma, HIV nephropathy, scleroderma, gout, renal tumour,

inborn errors of metabolism (e.g. Fabry’s disease).

Congenital/inherited: Polycystic kidney disease, Alport’s syndrome, congenital hypoplasia.

E P IDEMIOLOGY 

Incidence of end-stage CRF in England >110 per million population per

year. Higher incidence in Asian immigrants than native British population.

H ISTORY 

Anorexia, nausea, malaise, pruritus. Later: diarrhoea, drowsiness, convulsions,

coma.

Symptoms of the cause and other complications.

EXAMINA T I ON 

Systemic: Kussmaul’s breathing (acidosis), signs of anaemia, oedema,

pigmentation, scratch marks.

Hands: Leuconychia, brown line at distal end of nail.

There may be an arteriovenous fistula (buzzing lump in wrist or forearm).

Signs of complications (e.g. neuropathy, renal bone disease).

INVE S T I G A T IONS

 Blood: FBC (# Hb: normochromic, normocytic), U&E (# urea and

creatinine), eGFR (can be derived from creatinine and age using the MDRD calculator),

#Ca2þ

, " phosphate, AlkPhos, PTH.

Investigate for suspected aetiology: e.g. ANCA, ANA, glucose.

24-h urine collection: Protein, creatinine clearance (which is a rough estimate of GFR).

Imaging: Signs of osteomalacia and hyperparathyroidism. CXR may show pericardial effusion

or pulmonary oedema.

Renal ultrasound: Measure size, exclude obstruction and visualize structure.

Renal biopsy: For changes specific to the underlying disease, contraindicated for small kidneys.

MANAGEMENT

 Treat the underlying cause: Control diabetes

Manage complications of chronic kidney disease:

. Anaemia: Correct iron stores. Regular IV or SC erythropoietin (usually monthly).

. BP control: ACE inhibitors and Angiotensin-II antagonists (caution with renal artery stenosis).

. Hypocalcaemia: Maintain serum levels with 1-hydroxylated vitamin D analogues, e.g.

alfacalcidol. Consider bisphosphonates.

. Diet: High-energy intake, potassium intake restriction (in hyperkalaemia or acidosis,

oral NaHCO3 may be required), restriction of protein and phosphate intake (using

phosphate binders, e.g. calcium bicarbonate or aluminium hydroxide to # phosphate

absorption).

Renal failure (chronic) (continued)

. Drugs: Avoid nephrotoxic drugs (e.g. NSAIDs). Dose adjustments for drugs excreted from

kidneys.

. Oedema: Diuretics, e.g. furosemide (frusemide), metolazone.

Renal replacement therapy:

. Peritoneal dialysis (CAPD): Dialysate is introduced and exchanged through a ‘Tenkoff’

catheter, inserted via a subcutaneous tunnel into the peritoneum.

. Haemodialysis: Blood is removed via an arteriovenous fistula surgically constructed in the

wrist or forearm to provide high flow. Uraemic toxins are removed by diffusion across a

semipermeable membrane in an extracorporeal circuit (this may activate coagulation so

patients are heparinized).

. Renal transplantation: Requires long-term immunosuppressants to # rejection (e.g.

steroids, ciclosporin A, tacrolimus, azathioprine, daclizumab).

COMPL I C A T IONS 

Haematological: Anaemia (# erythropoietin production, # marrow

activity, # RBC survival, # dietary Fe/folate, " blood loss: haemodialysis/sampling),

abnormal platelet activity (bruising, epistaxis).

CVS: Accelerated atherosclerosis, " BP, pericarditis.

Neuromuscular: Peripheral & autonomic neuropathy, myopathy.

Renal osteodystrophy: Osteoporosis, osteomalacia (# 1a-hydroxylation of vitamin D), secondary

or tertiary hyperparathyroidism, adynamic bone disease (# bone turnover and

fractures secondary to excessive suppression of the parathyroid gland with current

therapies), osteosclerosis.

Endocrine: Amenorrhoea, erectile impotence, infertility.

Peritoneal dialysis: Peritonitis (e.g. staphylococcus epidermidis).

Haemodialysis:

. Acute: Hypotension (excessive removal of extracellular fluid).

. Long-term:

* Atherosclerosis.

* Sepsis (secondary to peritonitis, Staph. aureus infection).

* Amyloidosis: Failure of removal of b2-microglobulin (component of HLA molecules) by

dialysis membranes ! periarticular deposition ! arthralgia (e.g. shoulder) and carpal

tunnel syndrome.

* Aluminum toxicity: Accumulation of aluminum from the dialysis fluid and phosphate

binders ! dementia, osteodystrophy, microcytic anaemia (rare).

Transplantation/immunosuppression: " BP, opportunistic infections (e.g. CMV), malignancies

(lymphomas and skin), recurrence of renal disease (e.g. Goodpasture’s syndrome), sideeffects

of drugs (e.g. steroids: features of iatrogenic Cushing’s syndrome; ciclosporin:

gum hyperplasia).

P ROGNOS I S 

Depends on complications. Timely dialysis and transplantation " survival.

0 تعليق

PH.Jafar Jassim 12/11/2020 10:29:00 م

تابع القراءه

Polycystic kidney disease (PKD)

D E FI N I T ION

 Autosomal dominant inherited disorder characterized by the development of

multiple renal cysts that gradually expand and replace normal kidney substance, variably

associated with extrarenal (liver and cardiovascular) abnormalities.

AE T IOLOGY

 Eighty five percent are mutations in PKD1 (polycystin-1) on chromosome 16,

a membrane-bound multidomain protein involved in cell–cell and cell–matrix interactions;

15% are mutations in PKD2 (polycystin-2) on chromosome 4, a Ca2þ

permeable

cation channel.

Pathological process is considered to be a proliferative/hyperplastic abnormality of the tubular

epithelium. In early stages, cysts are connected to the tubules from which they arise and

the fluid content is glomerular filtrate. When cyst diameter>2 mm, most detach from the

patent tubule and the fluid content is derived from secretions of the lining epithelium.

With time, cysts enlarge and cause progressive damage to adjacent functioning

nephrons.

E P IDEMIOLOGY

 Most commonly inherited kidney disorder affecting one in 800, responsible

for nearly 10% of end-stage renal failure in adults.

H ISTORY

 Usually present at 30–40 years. Twenty percent have no family history.

May be asymptomatic.

Pain in flanks as a result of cyst enlargement/bleeding, stone, blood clot migration,

infection.

Haematuria (may be gross).

Hypertension.

Associated with intracranial ‘berry’ aneurysms and may present with subarachnoid haemorrhage:

sudden onset headache.

EXAMINA T I ON 

Abdominal distension, enlarged cystic kidneys and liver palpable, hypertension.

Signs of chronic renal failure at late stage.

Signs of associated aortic aneurysm or aortic valve disease.

INVE S T I G A T IONS

 Ultrasound or CT imaging: Multiple cysts observed bilaterally in enlarged

kidneys, sensitivity of detection poor for those <20 years. Liver cysts may also be

seen.

MANAGEMENT 

Blood pressure control: Slows the rate of decline in renal function and

minimizes the risk of rupture of a cerebral aneurysm. ACE inhibitors can effectively # blood

pressure and minimize the degree of secondary glomerular injury by # intraglomerular

pressure.

Haematuria: Managed conservatively.

Infections: Prompt treatment with non-nephrotoxic antibiotics (ciprofloxacin or co-trimoxazole).

Avoid the use of NSAIDs.

End-stage renal failure: (see renal failure, chronic).

Consider screening for intracranial aneurysm if family history of aneurysm.

Surgery: Cyst decompression reserved for selected cases. Liver cyst aspiration, marsupialization

or resection if gives rise to pain.

Genetic counselling.

COM P L IC A T I ONS

 Chronic renal failure, renal stones (20%).

1–2% suffer subarachnoid haemorrhage/intracerebral bleed.

Cysts develop in the liver (70%) and pancreas (10%) but these rarely cause organ dysfunction.

Mitral valve prolapse, diverticulosis of the colon.

PROGNOSIS

 Fifty percent develop end-stage renal failure by age 60 years. Renal replacement

therapy prolongs life by 15 years (mean). Patients with hypertension are much more

likely to develop progressive renal failure.

NEPHROLOGY 125

0 تعليق

PH.Jafar Jassim 12/10/2020 03:34:00 ص

تابع القراءه

يجب أن يتمتع بالثقافة الطبية حتى وإن لم يكن يكن طبيباً  ، والتي تعتبر الثقافة والمعرفة تعتبر عصباً لحياة الإنسان ، وصحة المجتمع الذي يعيش فيه ، وفي هذا المقال سوف تتذكر مجموعة معلومات عامة تختص في مجال الطب.

 من أهمّ الغدد في جسم الإنسان: الغدة الجنبدرقية ، والنخامية ، والدرقية ، والجنسية ، والمعدة ، والكظرية ، والعرقية ، والبنكرياس ، 

واللعابية. 

ينقل القمل للإنسان مرض اسمه التيفوس. 

الغدد الليمفاوية تعمل على تصفية الدم وتطهيره. يطلق عملية غسيل الكلى. 

يعدّ الكبد العضو الوحيد في جسم الإنسان الذي يعود للنمو بعد اقتطاع جزء منه. 

في العام 1989 م تمتت عملية زراعة الكبد في شيكاغو الأمريكية. 

مرض انفصام الشخصية اسمه مرض الشيزوفرينيا. فصيلة الدم

 o + تسمّى باسم فصيلة الدم الكريمة. 

تعرف الذبحة الصدرية بأنّها عبارة عن ألم حاد وقصير الوقت يحدث في الصدر وذلك بسبب إصابة الشريان التاجي. 

فيتامين الوحيد الذي يكسبه الجسم من أشعة الشمس هو فيتامين د. 

يبلغ وزن مخضر الإنسان البالغ من 3 إلى 2 كغم. 

الغدة التي تصبّ جميع محتوياتها بشكل مباشر في الدم هي الغدد الصماء. 

يؤدي نقص فيتامين أ للإصابة بمرض العشى الليليّ. 

من أعراض مرض البلاجرا: الغثيان ، والاكتئاب ، والصداع ، والإسهال ، والتهاب الجلد. 

يعتبر الطبيب العربي مجدي يعقوب من أشهر جراحي القلب على مستوى العالم ، وفردريك بانتينج مكتشف الإنسولين ، والطبيب العربي ابن زهر مكتشف جرثومة الجرب ، وسالك مكتشف مصل شلل الأطفال. يقصد بمرض السرطان الانقسام غير العادي لخلايا الجسم دون توقّف. 

وظيفة كريات الدم البيضاء هي الدفاع عن الجسم ضد الأمراض والجراثيم. 

تقع الغدة الدرقية في الرقبة. 

مادة الميلانين هي المسؤولة عن تلوين جسم الإنسان. 

تعدّ العضلات أثقل من العظام. 

يبلغ عدد فقرات العمود الفقري ثلاثاً وثلاثين فقرة. 

يعتبر مخ ّالمرأة أقل وزناً من مخّ الرجل. يبلغ عدد عظام الجمجمة اثنتين وعشرين عظمة. 

يبلغ حجم الهواء الذي يستنشقه الإنسان في كل عام خمسة ملايين لتر.

يبلغ عدد ضربات قلب الحوت ضربة واحدة في الدقيقة الواحدة. 

يبلغ عدد خلايا الجسم في الإنسان ستين ترليون خلية. 

يبلغ عدد الخلايا العصبية الذي يملكها الإنسان ثمانية وعشرين بليون خلية. 

المسؤول عن التذوق هي الحليمات الذوقية في اللسان. 

تعتبر عضلة الفخذ أكبر عضلة في الجسم ، وعضلة الركاب في الأذن الوسطى أصغر عضلة ، وعضلة الفكين أقوى عضلة. 

ضم المعدة تتكون من المخاط ، ولو لم تكن كذلك له ضمت نفسها .

1 تعليق

PH.Jafar Jassim 7/29/2020 12:19:00 ص

تابع القراءه