Dietary recommendations to minimize the formation of kidney stones include

increasing total fluid intake to achieve more than two liters per day of urine output;
limiting cola, including sugar-sweetened soft drinks; to less than one liter per week. limiting animal protein intake to no more than two meals daily (an association between animal protein and recurrence of kidney stones has been shown in men);
increasing citrate, or alkali intake, including from lemon and lime juice. However, citric acid does not alkalinize urine like alkali citrate, which is citrate bonded with sodium, potassium and magnesium. This is because when citrate is metabolized (mostly by liver and some by kidney), the protons in citric acid will neutralize the bicarbonate generated, so that no net effect on blood or urine pH will occur. Reducing sodium intake is associated with a reduction in urine calcium excretion.Maintenance of dilute urine by means of vigorous fluid therapy is beneficial in all forms of kidney stones, so increasing urine volume is a key principle for the prevention of kidney stones. Fluid intake should be sufficient to maintain a urine output of at least 2 litres (68 US fl oz) per day. A high fluid intake may reduce the likelihood of kidney stone recurrence or may increase the time between stone development without unwanted effects. Calcium binds with available oxalate in the gastrointestinal tract, thereby preventing its absorption into the bloodstream. Reducing oxalate absorption decreases kidney stone risk in susceptible people.
Based on one study, it has the highest affinity for the norepinephrine transporter (NET) of any other TCA, and is said to be the most noradrenergic and the most selective for the NET of the TCAs. The observed effectiveness of desipramine in the treatment of ADHD was the basis for the development of the selective NRI atomoxetine and its use in ADHD.Desipramine has the weakest antihistamine and anticholinergic effects of the TCAs. It tends to be slightly activating/stimulating rather than sedating, unlike most others TCAs. Whereas other TCAs are useful for treating insomnia, desipramine can cause insomnia as a side effect due to its activating properties. The drug is also not associated with weight gain, in contrast to many other TCAs. Secondary amine TCAs like desipramine and nortriptyline have a lower risk of orthostatic hypotension than other TCAs, although desipramine can still cause moderate orthostatic hypotension. Pharmacokinetics
Desipramine is the major metabolite of imipramine and lofepramine. Chemistry
Desipramine is a tricyclic compound, specifically a dibenzazepine, and possesses three rings fused together with a side chain attached in its chemical structure. Other dibenzazepine TCAs include imipramine (N-methyldesipramine), clomipramine, trimipramine, and lofepramine (N-(4-chlorobenzoylmethyl)desipramine). Desipramine is a secondary amine TCA, with its N-methylated parent imipramine being a tertiary amine. Other secondary amine TCAs include nortriptyline and protriptyline. The chemical name of desipramine is 3-(10,11-dihydro-5H-dibenzo[b,f]azepin-5-yl)-N-methylpropan-1-amine and its free base form has a chemical formula of C18H22N2 with a molecular weight of 266.381 g/mol.