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    Nephrology: Omar K MRCP Ireland

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    Manmeet S
    This document summarizes key topics in nephrology including acute kidney injury, chronic kidney disease, renal replacement therapies like hemodialysis and peritoneal dialysis, kidney transplantation complications, glomerulonephritis, nephritic syndrome, diuretics, rhabdomyolysis, renal tubular acidosis, and autosomal dominant polycystic kidney disease. It provides definitions, causes, tests, and treatments for each topic.

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    Nephrology: Omar K MRCP Ireland

    Uploaded by

    Manmeet S
    60 views54 pages
    This document summarizes key topics in nephrology including acute kidney injury, chronic kidney disease, renal replacement therapies like hemodialysis and peritoneal dialysis, kidney transplantation complications, glomerulonephritis, nephritic syndrome, diuretics, rhabdomyolysis, renal tubular acidosis, and autosomal dominant polycystic kidney disease. It provides definitions, causes, tests, and treatments for each topic.

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    5.Nephrology

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    This document summarizes key topics in nephrology including acute kidney injury, chronic kidney disease, renal replacement therapies like hemodialysis and peritoneal dialysis, kidney transplantation complications, glomerulonephritis, nephritic syndrome, diuretics, rhabdomyolysis, renal tubular acidosis, and autosomal dominant polycystic kidney disease. It provides definitions, causes, tests, and treatments for each topic.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    60 views54 pages

    Nephrology: Omar K MRCP Ireland

    Uploaded by

    Manmeet S
    This document summarizes key topics in nephrology including acute kidney injury, chronic kidney disease, renal replacement therapies like hemodialysis and peritoneal dialysis, kidney transplantation complications, glomerulonephritis, nephritic syndrome, diuretics, rhabdomyolysis, renal tubular acidosis, and autosomal dominant polycystic kidney disease. It provides definitions, causes, tests, and treatments for each topic.

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    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    of 54

    Nephrology

    Omar K
    MRCP Ireland
    Acute kidney injury (AKI):
    • Rise in creatinine >26μmol/L in 48hrs
    • • Rise in creatinine >1.5 ≈ baseline
    • • Urine output <0.5mL/kg/h for >6
    consecutive hours.
    causes
    • 1_prerenal (azotemia)
    • renal hypoperfusion, eg hypotension (any
    cause, including hypovolaemia, sepsis), renal
    artery stenosis ± ACE-i.
    • 2_renal Intrinsic (ATN,GN,Infilit)
    • 3_post Post-renal
    Click to add title
    • Is the injury acute or the damage chronic?

    • Suspect chronic if small kidneys (<9cm) on


    USS, anaemia, low Ca2+, high PO4 3 –,
    • Indications for dialysis
    • 1_ Refractory pulmonary oedema
    • 2_Persistent hyperkalaemia (K+ >7mmol/L)
    • 3_Severe metabolic acidosis (pH<7.2 or base excess
    <10)
    • 4_Uraemic complications such as encephalopathy or
    Uraemic pericarditis (pericardial rub)
    5_ Drug overdose—BLAST: Barbituates, Lithium,
    Alcohol (and ethylene glycol), Salicylates, Theophyline,
    Cx of AKI
    • Hyperkalaemia
    • • Pulmonary oedema
    • • Uraemia—may require dialysis if severe or
    complications, eg encephalopathy,
    pericarditis, contact renal team.
    • • Acidaemia—may require dialysis, consider
    sodium bicarbonate orally or IV if in HDU/ICU
    CKD
    • Impaired renal function for >3 months based
    on abnormal structure or function,

    • or GFR <60mL/min/1.73m2 for >3 months


    with or without evidence of kidney damage.
    CKD mx
    • Tx the cause (HT,GN,post)

    • A anemia,acidosis
    • B Bp (target) Target BP is <130/80 (<125/75
    if diabetic or ACR >70)
    • C Ca (Renal bone disease) + electrolytes
    • D diet + diuretics
    RRT
    • 1_HD
    • 2_HF
    • 3_PD

    Complications of RRT
    1_mortality is ~20%, mostly due to cardiovascular disease: MI and CVA are much commoner in
    dialysis patients, thought due to a combinationof hypertension and calcium/phosphate
    dysregulation.
    2_Protein-calorie malnutrition is common in HD and is associated with morbidity and mortality.
    3_Renal bone disease: high bone turnover, renal osteodystrophy and osteitis fibrosa (due to high
    PTH).
    4_Infection: Uraemia causes granulocyte dysfunction.
    5_Amyloid accumulates in long–term dialysis patients and may cause carpal tunnel syndrome,
    arthralgia, and fractures.
    6_Malignancy is commoner in dialysis patients; this may be related to the cause of ESRF, eg
    urothelial tumours in analgesic nephropathy
    Renal tx
    • DCD
    • DBD
    • LD
    Cx of tx
    1_Surgical: Bleed, thrombosis, infection, urinary leaks, lymphocele, hernia.
    2_Delayed graft function :Usually ATN in graft due to ischaemia-reperfusion injury.
    3_Rejection: Can be acute or chronic. (Chronic allograft nephropathy) is the new
    terminology for chronic rejection.
    4_Drug toxicity: Neurological (tremor, confusion with CNIs), new onset diabetes
    after transplant (NODAT), gum hypertrophy and hirsutism (ciclosporin),
    agranulocytosis and hepatitis (antimetabolites).
    5_Infection: Increased risk of all infections, but opportunists and viral infections
    particularly due to poor T cell response. HSV, Candida, Pneumocystis jirovecii, CMV.
    6_Malignancy: 5-fold increased risk of cancer with immunosuppression,
    particularly skin and viral associated. Women should have regular cervical smears,
    7_Cardiovascular disease:
    GN
    GN
    • 1_IgA Np
    • Young
    • man with episodic macroscopic haematuria
    • tx: BP control with ACE-i. With nephritic
    presentation immunosuppression may slow
    decline of renal function

    • HSP (systemic iga Np)


    GN
    • Anti-glomerular basement membrane (GBM)
    disease (GOOD) STEROIDS
    • Post-streptococcal GN (a diffuse proliferative
    GN) SYMPTX
    • Rapidly progressive GN (ctd + VASCULITIS)
    STEROIDS
    N.Syn
    • Definition ? POH

    Complications
    • 1_Susceptibility to infection•
    • 2_Thromboembolism: (Up to 40%): eg DVT/PE,
    renal vein thrombosis.
    • 3_• Hyperlipidaemia:
    N.Syndr
    • 1_m.changes ? Tx?
    • 2_Membranous nephropathy tx (acei + fluids)
    • 3_ M.C 2types , tx
    • 4_Focal segmental glomerulosclerosis (FSGS)
    Tx steroids
    Diuretics and their
    mechanism of action
    • 1_Loop diuretics, eg furosemide, bumetanide
    Block the Na+/K+/2ClΩ co-transporter in the thick
    ascending limb of the Loop of Henle,
    2_Thiazide diuretics, eg bendrofl umethiazide,
    indapamide, metolazone
    They inhibit the Na+Cl transporter in the distal
    convoluted tubule
    3_Potassium-sparing diuretics Spironolactone and
    eplerenone are aldosterone antagonists (inhibit the
    sodium-retaining)
    • 4_Osmotic diuretics Mannitol
    • 5_Carbonic anhydrase inhibitors such as
    acetazolamide act on the proximal tubule to
    increase excretion of bicarbonate and on
    sequently sodium
    Interstitial nephritides
    • Tubulointerstitial nephritis (TIN) Infl ammation
    of the renal interstitium
    • Acute immune reaction to drugs,
    • infections or autoimmune disorders

    • Chronic
    Rhabdomyolysis
    • skeletal muscle breakdown
    • myoglobin, K+, PO4 3–, urate and creatine
    kinase (CK).
    • Complications include hyper K+ and AKI:
    myoglobin is filtered by the glomeruli and
    • precipitates, obstructing renal tubules.
    Causes
    • Causes: Many, including
    • post-ischaemia; eg embolism, clamp on artery during
    surgery, trauma: prolonged immobilization(eg after falling),
    burns, crush injury, excessive exercise, uncontrolled seizures;
    • drugs and toxins: statins, alcohol, ecstasy, heroin, snake bite,
    carbon monoxide, neuroleptic malignant syndrome (p855);
    • infections: Coxsackie, EBV, infl uenza;
    • myositis, malignant hyperpyrexia; inherited muscle
    • disorders: McArdle’s disease, Duchenne’s muscular
    dystrophy
    • Tests: Plasma CK >1000iU/L (often
    >10,000iU/L).
    • K+ inc, PO4 3–inc, Ca2+ (enters muscle),
    urateinc.
    • AKI occurs 12–24 hours later, and DIC
    tx
    • 1_hyperkalaemia.
    • 2_IV fl uid rehydration is a priority to prevent AKI:
    maintain urine output at 300mL/h CVP monitoring is
    useful to prevent fl uid overload.
    • 3_IV sodium bicarbonate is used to alkalinize urine to
    pH >6.5, to stabilize a less toxic form of myoglobin.
    • 4_ Dialysis may be needed. Ideally manage patient in
    HDU/ICU setting to allow early detection of
    deterioration and regular bloods and
    monitoring. Prognosis is good if treated early.
    Renal tubular disease (RTA)
    • Renal tubular acidosis (RTA1)
    • Type 1 (distal) is due to an inability to excrete H+
    • Causes: Inherited disorders, acquired include
    SLE, Sjogren’s and drug related amphotericin).
    • Cx Nephrocalcinosis
    • Tests :Urine pH >5.5 despite metabolic acidosis.
    • Oral sodium bicarbonate
    Renal tubular disease (RTA)
    Type 2 (proximal) RTA is due to a ‘bicarbonate leak’: a defect in HCO3 –
    reabsorption in the proximal tubule resulting in excess HCO3
    in the urine (pH <5.5) leading to a metabolic acidosis.
    Type 2 RTA
    (Fanconi syndrome,

    . Hypokalaemia is common,
    . Diagnosis: IV sodium bicarbonate load: there is a high fractional
    excretion of HCO3 – (>15%).

    Treatment: High doses of bicarbonate (>10mmol/ kg/day) are required.


    • APCKD

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