Renal Tubule Disorders

This is a group of disorders which can affect specific parts of the nephron, leading to specific symptoms.

– The symptoms reflect an inability to reabsorb or excess reabsorption of solutes in the various segments.

Fanconi syndrome

This is a disorder causing impairment of PCT function, preventing solute reabsorption


– Glycosuria + aminoaciduria + uricosuria + phosphateuria

– Loss of phosphate in the urine can cause bone demineralization giving osteomalacia


Replace phosphate

Bartter syndrome

This is an impairment of salt reabsorption in the thick ascending loop of Henle

– Sodium concentration increases further in the DCT increasing gradient for exchange with K+ and H+

– The severe loss of electrolytes can affect growth in children, the age-group it usually affects


These mimic loop diuretic effects –> Hypokalemia, hypochloremia + Metabolic alkalosis


Salt replacement + NSAIDs (stop prostaglandins antagonizing action of ADH)

Gitelman syndrome

This is an impairment of the NaCl cotransporter in the DCT

– This is milder than Bartter syndrome –> presents in adulthood with incidental findings


Mimic thiazide diuretic effects –> hypokalemia, metabolic alkalosis, gout


Electrolyte supplementation

Renal Tubular Acidosis (RTA)

This is a condition involving accumulation of acid in the body, due to a failure of the kidneys to acidify the urine.

– RTA only used for patients with poor urinary acidification but otherwise well-functioning kidneys

– Can be caused by inability to excrete H+ ions, or inability to reabsorb HCO3 in the PCT.

i) Type 1:

This is a failure of H+ excretion from distal parts of nephron, due to dysfunction of H+/K+ antiporter


Genetic disease or secondary to autoimmune/toxins


– Gives hypokalemia, hypocalcaemia and hyperchloremia

– High acid demineralizes bone (osteomalacia)

– High Ca2+ in urine gives urinary stone + nephrocalcinosis (Kidney Ca2+ deposition)

– Urine is not acidified


HCO3– replacement to buffer acid and treat underlying disease


ii) Type 2:

This is a failure of HCO3 reabsorption in the PCT, giving urinary HCO3 loss and metabolic acidosis

– Loss of HCO3 means that Na+ is held back as major cation, increasing gradient for K+ loss

– However, the distal intercalated cells still work, so the acidosis is less severe than type 1


Heavy metals, drugs –> usually accompanied with Fanconi syndrome


Acidosis demineralizes bone + hypokalemia


HCO3 and K+ replacement


iii) Type 3:

This is a combination of type 1 and 2 RTA which occurs in children


iv) Type 4:

This is a secondary RTA which is due to hypoaldosteronism


Aldosterone deficiency or resistance (due to drugs e.g. K+ sparing diuretic)


Gives hyperkalaemia, hypotension and metabolic acidosis

Acute Tubular Necrosis (ATN)

This is a condition giving necrosis death of the tubule lining cells

– The necrotic cells fall off and can then obstruct the tubules decreasing the GFR


– Poor renal blood flow (hypovolaemic/septic shock)

– Drugs –> NSAIDs, aminoglycoside antibiotics, iodine

– Heavy metal poisoning –> lead

– Endogenous agents –> Urate (breakdown of tumour cells), so allopurinol used before chemotherapy to reduce urate-induced ATN


– Oliguria phase followed by polyuria phase

– AKI –> Poor urine output with raised urea and creatinine

– Hyperkalemia with metabolic acidosis

– Muddy brown, granular casts in urine is key


– Hydration and cessation of nephrotoxic substance

– Recovery is seen within 1-3 weeks as the PCT cells are constantly replaced

Acute interstitial nephritis (ATIN)

This is a hypersensitivity reaction which causes inflammation of the nephron and the surrounding interstitial space


– Drugs (NSAIDs, penicillin, diuretics, allopurinol)

– Infection by Staphylococci or underlying connective tissue diseases


– Signs of an allergy with rash and fever

Joint paint

Renal dysfunction –> Oliguria (low urine) + azotemia + Hypertension

– Key is eosinophilia which demonstrates that it is an allergic mediated inflammatory reaction


Sterile pyuria + white cell casts seen in the urine


Stop causative agent and can give steroids


It can be confusing to distinguish between ATN and ATIN:

– In ATN, there is blood AND protein found in the urine. In addition, there are similar levels of blood cells as WCC seen in the urine

– In ATIN, there can be both blood and protein found in the urine too. However, as it is a hypersensitivity reaction, there are more WCCs than blood cells in the urine

Chronic interstitial nephritis (CTIN)

This is a chronic condition of the interstitium and tubules

– Chronic inflammatory episodes eventually lead to fibrosis of the tubules impairing kidney function

– If left untreated, these patients will eventually suffer from chronic kidney disease


Most commonly due to drugs or infection


Stop causative agent and treat the progressive CKD