Lateral meniscal root tears occur in approximately 7% of ACL injured knees

Pathophysiology
The force distribution is across the knee joint, increasing force concentration on the cartilage and other joint structures.Damage to the meniscus due to rotational forces directed to a flexed knee (as may occur with twisting sports) is the usual underlying mechanism of injury. A valgus force applied to a flexed knee with the foot planted and the femur rotated externally can result in a lateral meniscus tear. A varus force applied to the flexed knee when the foot is planted and the femur rotated internally result in a tear of the medial meniscus.Tears produce rough surfaces inside the knee, which cause catching, locking, buckling, pain, or a combination of these symptoms. Abnormal loading patterns and rough surfaces inside the knee, especially when coupled with return to sports, significantly increase the risk of developing arthritis if not already present. Anatomy
The menisci are C-shaped wedges of fibrocartilage located between the tibial plateau and femoral condyles. The menisci contain 70% type I collagen. The larger semilunar medial meniscus is attached more firmly than the loosely fixed, more circular lateral meniscus. The anterior and posterior horns of both menisci are secured to the tibial plateaus. Anteriorly, the transverse ligament connects the 2 menisci; posteriorly, the meniscofemoral ligament helps stabilize the posterior horn of the lateral meniscus to the femoral condyle. The coronary ligaments connect the peripheral meniscal rim loosely to the tibia.
Primary aldosteronism will cause metabolic alkalosis and hypokalaemia, but hypertension will be present and serum renin will be low
EAST syndrome, though neurological features will predominate
Renal cysts and diabetes syndrome can cause hypomagnesaemia and hypocalcuria, but is distinguished by early onset chronic kidney disease and an autosomal dominant inheritance pattern of renal cysts and/or diabetes

Treatment
Most asymptomatic individuals with Gitelman syndrome can be monitored without medical treatment. Dietary modification of a high salt diet incorporated with, potassium and magnesium supplementation to normalize blood levels is the mainstay of treatment. Large doses of potassium and magnesium are often necessary to adequately replace the electrolytes lost in the urine. Diarrhea is a common side effect of oral magnesium which can make replacement by mouth difficult but dividing the dose to 3-4 times a day is better tolerated. Severe deficits of potassium and magnesium require intravenous replacement. If low blood potassium levels are not sufficiently replaced with replacement by mouth, aldosterone antagonists (such as spironolactone or eplerenone) or epithelial sodium channel blockers such as amiloride can be used to decrease urinary wasting of potassium.In patients with early onset of the disease such as infants and children, indomethacin is the drug of choice utilized to treat growth disturbances. Indomethacin in a study by Blanchard et al. 2015 was shown to increase serum potassium levels, and decrease renin concentration. Adverse effects of indomethacin include a decrease in the glomerular filtration rate, and gastrointestinal disturbances.Cardiac evaluation is promoted in the prevention of dysrhythmias and monitoring of QT interval activity.