there are two major components to the diagnostic evaluation:

Assessment of urinary potassium excretion to distinguish renal potassium losses (eg, diuretic therapy, primary aldosteronism) from other causes of hypokalemia (eg, gastrointestinal losses, transcellular potassium shifts).Assessment of acid-base status, since some causes of hypokalemia are associated with metabolic alkalosis or metabolic acidosis.

A 24-hour urine collection is the most accurate method to measure urinary potassium excretion. A normal individual can, in the presence of potassium depletion that is not due to urinary losses, lower urinary potassium excretion below 25 to 30 mEq per day on a 24-hour urine collection . Higher values suggest at least a contribution from urinary potassium wasting.ince creatinine is excreted at a near-constant rate, the urine potassium-to-creatinine ratio corrects for variations in urine volume. The urine potassium-to-creatinine ratio is usually less than 13 mEq/g creatinine (1.5 mEq/mmol creatinine) when hypokalemia is caused by transcellular potassium shifts, gastrointestinal losses, previous use of diuretics, or poor dietary intake . Higher values are seen with renal potassium wasting.

1. The diagnosis of RTA requires measurement of the urine pH and estimation of urinary ammonium excretion. The urine pH is persistently 5.5 or higher in patients with distal RTA. (  pH was 7.2 in this case) . The UAG (sometimes also called the "urine cation gap" or the "urine net charge") is calculated as the difference between the sum of the urine sodium plus potassium concentrations and the urine chloride concentration . The UAG can provide an indirect, or surrogate, estimate of urinary NH₄ excretion. A positive UAG that is 20 or greater is usually indicative of a low or normal NH₄ excretion. Thus, patients with metabolic acidosis due to impaired renal NH₄ excretion (such as a distal RTA) will have a positive UAG ( as in our patient ) .A negative UAG that is less than -20 is usually indicative of increased NH₄ excretion  UAG is generally between -20 and -50 mEq/L in patients with metabolic acidosis generated by diarrhea.

   An alternative method to qualitatively estimate the urine NH₄ concentration is the UOG. This calculation correlates well with urine NH₄ whether it is excreted with chloride or any other anion. Thus, the relationship between the UOG and NH₄ excretion is generally not disrupted by those conditions that will disrupt the relationship between urine NH₄ and the UAG. The UOG is calculated as the mathematical difference between the directly measured urine osmolality and the calculated urine osmolality derived from the urine concentrations of sodium, potassium, urea nitrogen (or urea), and, if the dipstick is glucose positive, glucose concentrations. Calculated urine osmolality (mosmol/kg)  =  (2  x  [Na + K]) + [urea nitrogen in mg/dL]/2.8 + [glucose in mg/dL]/18.•The major renal response to chronic metabolic acidosis is increased NH₄ excretion, and this may exceed 200 to 300 mEq/day in patients with chronic severe metabolic acidosis . Conversely, a value below 75 mEq/L in a patient with chronic metabolic acidosis suggests impairment in NH₄ excretion. A UOG of less than 150 mosmol/kg in a patient with chronic metabolic acidosis suggests that NH₄ excretion is impaired. Because NH₄ excretion is reduced in patients with distal RTA, a low UOG is consistent with this diagnosis. •When the UOG exceeds 400 mosmol/kg, it is likely that the urine NH₄ concentration is 200 mEq/L or greater. This would be expected with hyperchloremic metabolic acidosis generated by chronic diarrhea and other metabolic acidosis that are not due to renal tubular defects.

2. . Although vomiting can cause fluid loss directly from gastrointestinal tract, potassium depletion in this setting is primarily due to increased urinary losses  from the fact that concentration of potassium in gastric secretions is only 5 to 10 mEq/L. Loss of gastric acid induces metabolic alkalosis and high plasma bicarbonate level. Water and sodium bicarbonate are transported to the distal potassium secretory site. In addition, hypovolemia from vomiting induces increase in aldosterone release. These 2 effects increase renal potassium loss in the urine and cause hypokalemia
3. The urine pH in proximal RTA will be appropriately 5.3 or less if the filtered bicarbonate load is reduced and can be completely reabsorbed, which most often occurs in untreated patients( patient in this case not on chronic treatment)

4. type 4 renal tubular acidosis and appears to be due primarily to decreased urinary ammonium excretion and presents typically with   hyperchloremic acidosis) unless there is concurrent renal insufficiency. Reduced aldosterone secretion or aldosterone  resistance leads to  hyperkalemia and a mild hyperchloremic metabolic acidosis

Sjögren’s syndrome is an autoimmune condition which typically involves lymphocytic infiltration of the salivary, parotid and lacrimal glands, resulting in the characteristic symptoms of xerosis (dry eyes) and xerostomia (dry mouth). This immune process can also affect non-exocrine organs, such as the skin, lungs, gastrointestinal tract and the kidneys.Tubulointerstitial inflammation in the form of TIN is the most common renal manifestation of Sjögren’s syndrome. Depending on the segment of the nephron impacted by lymphocytic infiltration, TIN has been shown to manifest as hypokalaemia, acidosis, RTA (predominantly distal and rarely proximal), Gitelman syndrome, Fanconi syndrome and diabetes insipidus Similarly, it can also lead to nephrocalcinosis and renal calculi. Histological findings in RTA secondary to Sjögren’s are typically described as diffuse lymphocytic infiltration in the renal interstitial tissues, interspersed with plasma cells