Nephrology
eBook - ePub

Nephrology

A Comprehensive Guide to Renal Medicine

  1. English
  2. ePUB (mobile friendly)
  3. Available on iOS & Android
eBook - ePub

Nephrology

A Comprehensive Guide to Renal Medicine

About this book

Lecture Notes: Nephrology is a concise introduction to the fundamental principles of nephrology. An ideal study guide for medical trainees, this accessible resource combines the depth of a textbook with the accessibility of a handbook. Succinct chapters describe the clinical implications of renal physiology, examine major renal disorders and diseases, and explain a wide range of management and treatment options.

A new addition to the popular Lecture Notes series, this handbook provides trainees in nephrology with core subject knowledge and enables medical students to gain a more comprehensive understanding of this complex specialty.

  • Offers clear, easy-to-understand coverage of all relevant nephrology topics
  • Includes MCQs and discussion around the answers, ideal for those preparing for written Internal Medicine examinations, including the certification examination of the American Board of Internal Medicine, the UK-based MRCP and the Australia and New Zealand-based FRACP examinations
  • Features chapter summaries and numerous infographics, tables and figures
  • Emphasises core management skills needed by medical students and junior doctors
  • Is presented in the consistent and well-recognised Lecture Notes format

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Information

Year
2020
Print ISBN
9781119058045
eBook ISBN
9781119058113
Edition
1

1
Clinical Implications of Renal Physiology

Surjit Tarafdar

Summary

  • Besides maintaining a stable acid base, electrolyte, and fluid status of the body, kidneys also have an important endocrine role in producing and secreting 1,25‐dihydroxycholecalciferol (calcitriol), renin, and erythropoietin
  • More than 98% of water in the filtered urine is reabsorbed in the tubules; 90–95% of water is reabsorbed as it follows sodium (Na+), which is avidly reabsorbed by the Na+‐deficient epithelial cells, except in the collecting duct (CD), where 5–10% of water is reabsorbed (independent of Na+) under the direct influence of vasopressin or anti‐diuretic hormone (ADH)
  • The tubular epithelial cells constantly lose three Na+ and gain two potassium (K+) ions from the basolateral membrane (due to the Na+‐K+‐ATPase), which keeps these cells deficient in Na+
  • The countercurrent mechanism, which is dependent on the impermeability of the thick ascending limb (TAL) to water, leads to the creation of an increasing osmotic gradient from the cortex to the deeper medulla, which in turn enables ADH to reabsorb water in the CD
  • Aldosterone helps in Na+ reabsorption in the CD and also leads (directly) to K+ and (indirectly) to hydrogen (H+) secretion into urine
  • All diuretics act by inhibiting tubular reabsorption of Na+
  • Formation of urine begins in the glomerular capillaries where the filtrate has to cross the three filtration layers: endothelium, glomerular basement membrane (GBM) and the foot processes of the podocytes; all these three layers are negatively charged and hence repel anionic proteins like albumin
  • Nephrotic syndrome, which is marked by abnormally increased filtration of plasma proteins in the urine, may be due to widening of the pores in the three filtration layers, but is almost always associated with loss of negative charges in these layers
  • Nephritis, which is due to glomerular inflammation, is characterized by haematuria with red blood cell (RBC) casts and dysmorphic RBCs, some degree of oliguria, hypertension, and reduction in glomerular filtration rate
  • Goodpasture’s disease, which is characterized by antibodies against subtype of type IV collagen, can lead to nephritis and haemoptysis, as this particular collagen is found predominantly in the GBM and alveolar membranes of the lungs
  • Familial hypocalciuric hypercalcaemia, which manifests with hypercalcaemia, characteristically low urinary calcium and normal to high serum parathyroid hormone (PTH) level, is due to mutation in the calcium‐sensing receptor (found in the kidney and parathyroid gland) leading to abnormally increased renal reabsorption of calcium and inappropriate secretion of PTH
  • Distal renal tubular acidosis (type 1 RTA) is due to an inability of the distal tubules to excrete H+, whilst proximal renal tubular acidosis (type 2 RTA) is due to an inability of the proximal tubules to reabsorb bicarbonate (HCO3−)
  • Metabolic acidosis leads to hyperkalaemia and vice versa
The kidneys are paired retroperitoneal structures that are normally located between the transverse processes of the T12–L3 vertebrae, with the left kidney typically somewhat more superior in position than the right. Each kidney has an outer cortex and an inner medulla which protrudes into the pelvis. The pelvis is practically the funnel‐shaped dilated upper end of the ureter.
The kidney maintains a stable acid base, electrolyte, and fluid status inside the body by selective elimination or retention of water, electrolytes, and other solutes (Table 1.1). It does so by three mechanisms:
  1. Filtration of blood in the glomerulus to form an ultrafiltrate (water with low molecular weight solutes) which then enters the tubule.
  2. Selective reabsorption of water, electrolytes, and solutes from the tubules into the interstitium and peritubular capillaries.
  3. Selective secretion from the peritubular capillaries across the tubular epithelium into the tubular fluid.
Besides these mechanisms, the kidneys also play an active endocrine role by the production and secretion of:
  • 1,25‐dihydroxycholecalciferol: cholecalciferol is derived f...

Table of contents

  1. Cover
  2. Table of Contents
  3. List of Contributors
  4. Foreword
  5. Acknowledgements
  6. 1 Clinical Implications of Renal Physiology
  7. Questions and Answers
  8. 2 Investigation of Renal Diseases
  9. Questions and Answers
  10. 3 Disorders of the Renal Tubules Leading to Disturbances of Acid–Base and Potassium
  11. Questions and Answers
  12. 4 Renal Stones
  13. Questions and Answers
  14. 5 Kidney Cancer
  15. Questions and Answers
  16. 6 Acute Kidney Injury
  17. Questions and Answers
  18. 7 Chronic Kidney Disease
  19. Questions and Answers
  20. 8 Nephrotic Syndrome
  21. Questions and Answers
  22. 9 Glomerulonephritis
  23. Questions and Answers
  24. 10 Renal Vasculitis and Lupus Nephritis
  25. Questions and Answers
  26. 11 Renovascular Hypertension, Pregnancy‐Related Hypertension, and Thrombotic Microangiopathies
  27. Questions and Answers
  28. 12 Hereditary and Familial Renal Diseases
  29. Questions and Answers
  30. 13 Hepatorenal Syndrome
  31. Questions and Answers
  32. 14 Infections of the Kidney
  33. Questions and Answers
  34. 15 Diabetic Nephropathy
  35. Questions and Answers
  36. 16 Kidney Disease in Myeloma and Other Monoclonal Gammopathies
  37. Questions and Answers
  38. 17 Tubulointerstitial Diseases
  39. Questions and Answers
  40. 18 Maintenance Haemodialysis
  41. Questions and Answers
  42. 19 Peritoneal Dialysis: Principles, Indications, and Common Complications
  43. Questions and Answers
  44. 20 Renal Transplantation
  45. Questions and Answers
  46. Index
  47. End User License Agreement

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